![11
Failure to fully implement better nutritional knowledge and understanding
This failure to fully realise the benefits of better
nutrition knowledge is not confined to developing
countries.
In the UK many people have intakes of an
essential vitamin or mineral that are classified as
inadequate i.e. more than two standard deviations
below the estimated average requirement (termed
the lower reference nutrient intake [LRNI] in the
UK). There are also many people who have bio-
chemical indicators of nutrient status that are
below the minimum thresholds used to indicate
adequacy.
• According to a major UK report on iron and
health, over half of institutionalised elderly
people had blood haemoglobin levels indicative
of iron deficiency anaemia, and even in the
free-living elderly, anaemia rates ranged from
6% of women aged 65–74 years to 38% of men
aged over 85 years (anaemia rates are higher
in men than women in the elderly). The same
report found that 9% of adolescent girls were
anaemic, 24% had depleted iron stores (low
serum ferritin) and 48% had total iron intakes
below the LRNI (see Chapter 16).
• In 2012–2013 there were well over 800
admissions of children to British hospital for
rickets (vitamin D deficiency) and during the
winter months well over 30% of UK adults are
below the biochemical threshold indicative of
vitamin D inadequacy; double this number
if the higher threshold used by the American
Institute of Medicine is used (see Chapter 15).
• Many British women and girls have inadequate
iodine intake; perhaps half of teenaged girls
have urinary iodine concentrations indicative
of at least mild iodine deficiency There is
preliminary evidence that poor iodine status of
pregnant UK women is adversely affecting the
intellectual development of their offspring (see
Chapter 17).
Clear evidence has existed since 1991 that daily sup-
plements (400 µg) of folic acid (vitamin B9) taken from
before conception and in early pregnancy reduce the
incidence of neural tube defects, like anencephaly
and spinal bifida, in babies by around three quarters.
Yet advising women to take over-the-counter sup-
plements when planning a pregnancy has had little
impact on the rates of neural tube defects. In 1998,
the US and Canadian authorities introduced manda-
tory fortification of flour with folic acid and this led
to immediate and substantial falls in the incidence
of these neural tube defects. Over eighty countries
have followed this North American lead but despite
repeated recommendations from expert bodies, UK
and other European governments have resisted
introducing similar measures and this has resulted
in thousands of avoidable stillbirths, infant deaths,
terminations and births of severely disabled babies
(see Chapter 13).
The first British report to set quantitative targets
for dietary changes that would reduce the risks of
chronic degenerative disease (the National Advisory
Committee for Nutrition Education [NACNE]
report) was produced in 1983. It set some targets that
it envisaged could be achieved within 5 years, i.e. by
1988, and also more ambitious targets that might
take 15 years to be reached, i.e. by 1998. It set a 5-year
target for reducing the proportion of dietary energy
that should come from fat to no more than 35%. This
target re-appeared in the Department of Health’s
Health of the Nation report as a target for 2005, and
data from National Diet and Nutrition Survey sug-
gest that this preliminary NACNE target may actu-
ally have been reached in around 2010 i.e. more than
20 years later than envisaged by NACNE. In 1990 the
WHO made a recommendation that we should eat
5×80 g portions of fruit and vegetables each day and
this resulted in campaigns to promote 5 a day in sev-
eral countries, including the UK (in 2003). Despite
these WHO recommendations being made over 25
years ago and an active 5 a day campaign in the UK
since 2003, most British adults are still eating less
than 3 portions per day. In about 15 years the 5 a day
campaign has had only a small impact on the average
consumption of fruit and vegetables.
The examples in the previous paragraph suggest
that major improvements in nutritional health in
both industrialised and developing countries are not
now being held back primarily by a lack of scientific
knowledge and understanding but by economic and
political factors and a lack of compliance with nutri-
tional advice and guidelines.
Major and relatively costly vaccination and pub-
lic health programmes have had a major worldwide
impact in reducing the toll of some diseases. Such](https://image.slidesharecdn.com/28662727-250517223428-b4a3afb9/85/Nutrition-Maintaining-And-Improving-Health-Geoffrey-P-Webb-46-320.jpg)
![[1] Late Ashfield.
[2] Late Caistor.
[3] Late Lippincott.
[4] Closed during winter.
[5] Late Bentinck.
[6] Open during summer only.
[7] Late Artemesia.
[8] Late Cavagnol.
[9] Late Proton.
[10] Late Irish Creek.
[11] Late Glenelg.
[12] Formerly Merton.
[13] Late St. Vincent.
[14] Late Newland.
[15] Formerly Tring.](https://image.slidesharecdn.com/28662727-250517223428-b4a3afb9/85/Nutrition-Maintaining-And-Improving-Health-Geoffrey-P-Webb-65-320.jpg)
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- 9. CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2020 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works International Standard Book Number-13: 978-0-3673-6939-2 (Hardback) International Standard Book Number-13: 978-0-8153-6241-8 (Paperback) This book contains information obtained from authentic and highly regarded sources. Reasonable efforts have been made to publish reliable data and information, but the author and publisher cannot assume responsibility for the validity of all materials or the con- sequences of their use. The authors and publishers have attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Visit the Taylor & Francis Website at http://www.taylorandfrancis.com and the CRC Press Website at http://www.crcpress.com
- 10. For Kate and Lucy
- 12. vii Contents Preface xxiii Acknowledgement xxvii About the author xxix PART 1 CONCEPTS AND PRINCIPLES 1 1 Changing priorities in nutrition 3 Ensuring adequacy and use of food groups 3 A new priority – reducing the chronic diseases of ageing populations 6 Plates and pyramids: food guides to reflect modern nutritional priorities 7 Failure to fully implement better nutritional knowledge and understanding 9 The future of nutrition research 12 Yoghurt and ovarian cancer? A case study of unproductive research 14 Key reference 17 2 Food selection 19 Introduction and aims of the chapter 19 The biological model of food 20 Dietary and cultural prejudice 21 Food classification systems 22 Nutritional classification 22 Consumer classification 23 Anthropological classification of foods 25 Non-nutritional uses of food 27 Religion, morality and ethics 27 Status and wealth 27 Interpersonal relationships 27 Political 28 Folk medicine 28 The hierarchy of human needs 28 A model of food selection – “The hierarchy of availabilities model” 30 Physical availability 32 Economic availability 32 International trends 33 The problem of feeding the world 34 Effects of income upon food selection in the UK 36 Cultural availability 37 Dietary taboos 38 Effects of migration upon eating habits 40 “Gatekeeper” limitations on availability 43 A social–ecological model for food and activity decisions 45 Key references 46
- 13. viii Contents 3 Methods of nutritional assessment and surveillance 47 Aims and introduction 47 Strategies for nutritional assessment 47 The general lack of valid and reliable measurements in nutrition 48 Measurement of food intake 49 Population or group methods 49 Individual methods 53 Retrospective methods 53 Prospective methods 54 Doubly labelled water (DLW) 56 Tables of food composition 58 Food table problems and errors 58 Dietary standards and nutrient requirements 60 Origins of dietary standards 60 Definitions and explanations 60 The uses of dietary standards 63 Inaccurate standards 64 Defining requirement 65 Deprivation studies 66 Radioactive tracer studies 66 Balance studies 67 Factorial methods 67 Measurement of blood or tissue levels 68 Biochemical markers 68 Biological markers 69 Animal experiments 69 Clinical signs for the assessment of nutritional status 70 Anthropometric assessment in adults 71 Uses of anthropometric assessment 72 Height and weight 73 The Body Mass Index 73 Alternatives to height 74 Skinfold calipers 74 Bioelectrical impedance (BIA) 75 Estimation of fatness from body density 76 An alternative method of measuring body volume (air displacement plethysmography or Bod Pod) 76 Body water content as a predictor of body fat content 76 Mid-arm circumference measures 77 Anthropometric assessment in children 77 Body mass index in children 78 Estimating fatness in animals 80 Biochemical assessment of nutritional status 81 Measurement of energy expenditure and metabolic rate 83 Comparisons of metabolic rates between individuals 85 Key references 86 4 Investigating links between diet and health outcomes 89 Aims and scope of the chapter 89
- 14. ix Contents Observation vs experimentation 89 Range and classification of the methods available 90 About statistics 92 Observational human studies 94 Geographical comparisons 94 Anomalous populations 95 Special groups 95 Time trends 95 Migration studies 96 Cross-sectional surveys 96 “Experiments” of nature 97 Case-control studies 97 Cohort studies 98 Association in observational studies does not prove cause and effect 99 Criteria for establishing cause and effect 101 Animal and in vitro experiments 102 Role of animal and in vitro experiments 102 Animal use in UK experiments 104 The rationale for using non-human species in medical research 104 In vitro experiments 104 Animal experiments 105 The potential of animal experiments to mislead human biologists 105 Different strategies of mice and people during cold exposure 106 The nutritional burden of pregnancy in mice and people 107 Species vary in the nutrients they require and their response to foreign chemicals 107 Human experimental studies 108 General design aims of human experimental studies 108 Classifying human experiments 108 Important technical terms 109 Random allocation 109 Double-blind, placebo-controlled 109 Crossover design vs parallel design 110 Risk factors and risk markers 110 Compliance and contamination 111 Some examples of human experimental studies 112 Watercress and cancer 112 Echinacea and cold symptoms 113 Fluoridated water and dental caries in children 113 Folic acid supplements and neural tube defects 113 Vitamin E (alpha-tocopherol), beta-carotene and the risk of lung cancer 113 Scoring clinical trials for quality 114 A warning about uncontrolled trials 114 Key references 115 5 Investigating links between diet and health – amalgamation, synthesis and decision making117 Aims and scope of the chapter 117 Meta-analysis 117 What is it? 117
- 15. x Contents Growth of meta-analysis 118 Summarising the results of a meta-analysis 119 Some general problems with meta-analysis 120 Decision-making and hierarchies of evidence 121 The basic dilemma 121 Harm from intervention based on inadequate evidence? 122 Harm from unduly delayed intervention? 122 Evidence hierarchies 123 National Institute for Health and Clinical Excellence (NICE) 126 The need to be critical of the latest published research findings 127 Why are so many research findings irreproducible? 128 Bias 129 The pressure to achieve statistical significance 129 Selective exclusion/inclusion of outlying results 130 Multiple analyses 130 Underpowered studies 131 Small effect size 131 Multiple modelling 132 Randomised controlled trials, the gold standard of evidence? 132 Are meta-analyses the platinum standard? 134 A footnote about research fraud 136 Key references 139 6 Dietary guidelines and recommendations 141 The range of “expert reports” and their consistency 141 Variations in the presentation of guidelines and recommendations 144 “Food” recommendations 145 Energy and body weight 146 Recommendations for fats, carbohydrates, protein and salt 146 UK Targets 146 Rationale 147 Alcohol 148 Changing UK alcohol recommendations 149 What do these guidelines mean in terms of real-life behaviour? 149 How does current consumption compare to the new guidelines? 149 The economic impacts of alcohol 150 The (apparent) alcohol–mortality J-curve? 151 Alcohol increases risk of cancer, liver disease and accidental death 152 Why are the 1995 and 2016 conclusions so different? 153 Summing up the alcohol debate 155 How do current UK diets compare with “ideal” intakes? 156 Willingness to change 157 Some barriers to dietary change 158 Aids to food selection 160 Concluding remarks 161 Key references 163
- 16. xi Contents PART 2 ENERGY, ENERGY BALANCE AND OBESITY 165 7 Introduction to energy aspects of nutrition 167 Units of energy 167 How are energy requirements estimated? 168 Variation in average energy requirements – general trends 170 The energy content of foods 172 Sources of dietary energy by nutrient 173 Energy density 176 Nutrient density 178 The sources of dietary energy by food groups 179 Starvation 180 The immediate causes of starvation 180 Physiological responses and adaptations 180 Some adverse consequences of starvation 182 Eating disorders 183 Anorexia nervosa: Characteristics and consequences 183 Bulimia nervosa and binge eating disorder 184 Incidence of eating disorders 185 Causes of eating disorders 185 Cachexia 187 Cancer anorexia cachexia syndrome 187 Key references 189 8 Energy balance and its regulation 191 Concept of energy balance 191 Is there physiological regulation of energy balance? 193 “Set point” theory 193 External influences that affect food intake 194 Physiological regulation of energy intake 194 Early work with experimental animals 194 Hypothalamic centres controlling feeding – a more recent perspective 195 Gut-fill cues 197 The glucostat theory 198 The lipostat or adipostat theory 198 The leptin story 200 Is energy expenditure regulated? 203 Key references 207 9 Obesity 209 Defining obesity 209 Prevalence of overweight and obesity 210 A worldwide perspective 212 Effects of ethnicity and social status upon obesity prevalence 214 Overweight and obesity in children 217 The consequences of obesity 220 The relationship between BMI and life expectancy 220 Obesity and the quality of life 222 Not all body fat is equally bad 224 Weight cycling 225
- 17. xii Contents Does high BMI directly cause an increase in mortality? 225 The metabolic syndrome or “syndrome X” 228 The causes of obesity 228 Nature or nurture? 229 A weakening link between hunger and eating? – The internal/external hypothesis and behaviour therapy 230 Variety of food and sensory specific satiety 232 Is fat more fattening than carbohydrate? 233 Inactivity as a cause of obesity 235 Prevention and treatment of obesity in populations 237 Adopting a “low-risk” lifestyle 237 Targeting anti-obesity measures or campaigns 239 Obesity treatment in individuals 240 Realistic rates of weight loss 240 The reducing diet 241 Alternative diets 241 The role of exercise 242 Are the obese less “vigilant”? 244 More “aggressive” treatments for obesity 245 Drug therapy 245 Appetite suppressants 245 Drugs that block digestion 246 Drugs based on gut hormones 247 Drugs that increase energy expenditure 247 Leptin and leptin analogues 247 Surgical treatment for obesity 247 Very Low Energy Diets (VLEDs) 248 Use of these more extreme treatments 249 Key references 250 PART 3 THE NUTRIENTS 253 10 Carbohydrates 255 Introduction 255 Nature, classification and metabolism of carbohydrates 256 Aerobic metabolism of pyruvic acid 258 Dietary sources of carbohydrate 258 Sugars 259 Lactose or milk sugar 260 Sucrose 260 The new UK “sugar tax” 261 Artificial sweeteners 263 “Calorie-free” sweeteners 263 Sugar replacers 265 Diet and dental health 266 Starches 269 Dietary fibre/NSP 270 Resistant starch 274
- 18. xiii Contents The glycaemic index (GI) and glycaemic load (GL) 276 Dietary fibre and other factors in the aetiology of bowel cancer and heart disease 277 Background 277 Possible mechanisms by which dietary factors may affect bowel cancer risk 278 Descriptive epidemiology 278 Case-control and cohort studies 280 What about fibre and heart disease? 280 Key references 282 11 Protein and amino acids 285 Traditional scientific aspects of protein nutrition 285 Introduction 285 Chemistry, digestion and metabolism 285 Amino acid metabolism 287 Intakes, dietary standards and food sources 288 Nitrogen balance 289 Estimation of protein content 289 The concept of nitrogen balance 289 Negative nitrogen balance 289 Requirements for balance 290 Positive nitrogen balance 290 Dietary adequacy for protein is not a major issue 291 Protein quality 293 Essential amino acids 293 Establishing the essential amino acids and quantifying requirements 294 Limiting amino acid 294 First- and second-class proteins 294 Mutual supplementation of protein 295 Measurement of protein quality 295 Do children need more protein than adults? 296 Absolute requirement 296 The relative requirement 297 The protein level/concentration needed in the diet 297 Reasons why the past protein needs of children were exaggerated (personal interpretation) 298 Protein quality is probably of little significance in human nutrition 299 Conclusions 299 The protein gap – one of the biggest errors in nutritional science? 299 Overview 299 Aims of this section 300 Past belief in a protein gap and major initiatives taken to close this gap 300 The concept of a protein gap loses credibility 301 What caused the protein gap mistake? 302 Exaggerated estimates of the protein needs of children 302 Kwashiorkor, due to primary protein deficiency, is the dominant form of worldwide malnutrition? 303 Lasting impact of the protein gap myth 303 Concluding remarks 305 Key references 305
- 19. xiv Contents 12 Fat307 Nature of dietary fat 307 Types of fatty acids 309 Saturated fatty acids 309 Monounsaturated fatty acids 309 Polyunsaturated fatty acids 309 Cis/trans isomerisation 310 Effects of chain length and degree of unsaturation upon fatty acid melting points 310 Conjugated linoleic acid (CLA) 311 Distribution of fatty acid types in dietary fat 312 Polyunsaturates: saturates (P:S) ratio 313 Sources of fat in the diet 314 UK fat intakes and their food sources 315 Roles of fat in the diet 316 Fat as an energy source 316 Palatability 317 Satiation 318 Fat-soluble vitamins 318 Essential fatty acids 319 Essential fatty acids and eicosanoid production 320 Blood lipoproteins 322 Digestion, absorption and transport of dietary lipids 323 Transport of endogenously produced lipids 324 Fat metabolism 326 Statins 326 The “diet-heart hypothesis” and its implication for dietary fats 329 Current “health images” of different dietary fats 332 What about saturated vegetable fats like coconut and palm oil? 333 Trans-fatty acids 334 Plant sterols 335 Review of the evidence for the diet-heart hypothesis 336 The key tenets of the diet-heart hypothesis 336 Evidence overview 337 Experimental studies 337 “Experiments of nature” 337 Cohort studies 338 Intervention trials and clinical trials 338 Fish oils 340 Overview 340 How might fish oils exert beneficial health effects? 340 Evidence that high fish oil consumption may reduce CHD 341 Conclusions and fish consumption recommendations 342 Other natural oils used as supplements 343 Key references 344 13 Dietary supplements and food fortification 347 An overview of food fortification 347 Definitions 347 Early successes 348
- 20. xv Contents Fortification in the UK 348 Folic acid (vitamin B9) in flour – a modern fortification success story 348 Time to update UK food fortification policy 351 An overview of dietary supplements 353 Definition and categories of dietary supplements 353 Size and breakdown of the supplement market 354 Overview of uses and potential hazards 354 Some rules and regulations 355 Vitamin and mineral supplements 357 Do vitamin and mineral supplements ensure adequacy? 357 Do micronutrient supplements reduce cancer, cardiovascular disease and increase life expectancy? 359 Do individual micronutrient supplements offer specific benefits? 359 Strategies for improving micronutrient adequacy 363 Natural fats and oils 364 The main “natural oil” supplements 364 Evening primrose and starflower/borage oils 364 Fish oils 365 Dietary supplements or natural medicines? 366 Natural metabolites as dietary supplements 368 Conditionally essential nutrients 368 L-Carnitine 369 Glucosamine and Chondroitin sulphate 369 Co-enzyme Q10 (CoQ10) or ubiquinone 370 Creatine 371 Alpha (α)-lipoic acid 371 Lecithin and choline 372 s-Adenosylmethionine 372 Natural extracts as dietary supplements 373 Secondary metabolites in plant extracts 373 Role of plant secondary metabolites in preventing/treating disease 375 Phytoestrogens 376 Garlic supplements 377 Others 378 Antioxidants and the oxidant theory of disease 379 The nature and effects of free radicals 379 Origins of free radicals 379 Physiological mechanisms to limit free radical damage 380 Situations that might increase damage by free radicals 381 Do high antioxidant intakes prevent heart disease, cancer and other chronic diseases? 384 Key references 388 14 Food as medicine 391 Fruit and vegetables five, seven, ten or even three portions per day? 391 Background 391 A flavour of the evidence underpinning the 5-a-day recommendation 392 Calls to change the 5-a-day recommendation 393 Can we justify increasing the 5-a-day recommendations? 397 Is 10-a-day a realistic recommendation? 397
- 21. xvi Contents Superfoods 398 What are “superfoods”? 398 What is the theoretical basis of claims for superfoods? 399 Examples of superfoods 400 The choice of which foods to classify as superfoods is biased 402 Conclusions 402 Functional foods 403 Phytoestrogens 404 Probiotics, prebiotics and synbiotics 405 Plant sterols or phtyosterols 408 Key references 410 15 The vitamins 413 Some general concepts and principles 413 What is a vitamin? 413 Classification 414 Vitamin deficiency diseases 415 Precursors and endogenous synthesis of vitamins 416 Circumstances that precipitate deficiency 416 A note about individual vitamins 417 Vitamin A – retinol 417 Key facts 417 Nature and sources of vitamin A 418 Functions 419 Requirements and assessment of vitamin A status 420 Deficiency states 420 Risk factors for deficiency 421 Benefits and risks of high intakes 421 Vitamin D – cholecalciferol 421 Key facts 421 Nature, sources and requirements for vitamin D 422 Functions of vitamin D 424 Acute deficiency states 425 Vitamin D, osteoporosis and non-bone conditions 426 Safely improving the vitamin D status of the population 426 Vitamin E – α-tocopherol 426 Key facts 426 Overview 427 Vitamin K – phylloquinone 427 Key facts 427 Overview 428 Thiamin – vitamin B1 429 Key facts 429 Nature and sources 429 Functions 429 Requirements and assessment of status 430 Deficiency states 430 Riboflavin – vitamin B2 431 Key facts 431
- 22. xvii Contents Nature and sources 432 Functions 432 Requirements and assessments of status 432 Riboflavin deficiency 432 Niacin – vitamin B3 432 Key facts 432 Nature and sources 433 Functions 434 Dietary requirements and assessment of status 434 Niacin deficiency 434 Vitamin B6 – pyridoxine 435 Key facts 435 Nature and sources 435 Functions 436 Requirements and assessment of status 436 Deficiency and toxicity 436 Vitamin B12 – cobalamins 437 Key facts 437 Nature and sources 437 Functions 438 Requirements and assessment of status 438 Deficiency of B12 438 Folate or folic acid (vitamin B9) 438 Key facts 438 Nature and sources 439 Functions 440 Requirements and assessment of folate status 440 Folate deficiency 440 Folic acid and birth defects 441 Potential hazards of high folic acid intake 441 Biotin 441 Key facts 441 General overview 441 Pantothenic acid 442 Key facts 442 Vitamin C – ascorbic acid 442 Key facts 442 Nature and sources 443 Functions 443 Requirements and assessment of status 443 Deficiency states 443 Benefits and risks of high intakes 444 Key references 445 16 The minerals 447 Introduction 447 Chromium 448 Key facts 448 Overview 449
- 23. xviii Contents Copper 449 Key facts 449 Overview 449 Fluoride 450 Magnesium 451 Key facts 451 Overview 451 Manganese 451 Overview 452 Molybdenum 452 Key facts 452 Overview 452 Phosphorus 452 Potassium 453 Key facts 453 Overview 453 Selenium 454 Key facts 454 Overview 454 Zinc 455 Key facts 455 Overview 455 Iodine and iodine deficiency diseases 457 Key facts 457 Distribution and physiological function of body iodine 457 Iodine deficiency 457 Epidemiology of iodine deficiency across the world 458 Iodine in the UK and other affluent countries 459 High intakes and goitrogens in food 460 Iron and iron deficiency anaemia 461 Iron nutrition 461 Key facts 461 Distribution of body iron 462 Requirement for dietary iron 462 Regulation of iron balance and iron overload 463 Determination of iron status 463 Iron deficiency 464 Prevalence of iron deficiency and anaemia 464 Preventing iron deficiency 465 Calcium, diet and osteoporosis 467 Key facts 467 Distribution and functions of body calcium 467 Hormonal regulation of calcium homeostasis 468 Requirement and availability of calcium 468 Calcium and bone health 470 The nature of bone 470 Effects of age and sex upon bone density and fracture risk 470 Incidence of osteoporosis 472
- 24. xix Contents General and lifestyle risk factors for osteoporosis 472 Dietary risk factors for osteoporosis 474 Prevention and treatment of osteoporosis 474 Diet and lifestyle conclusions 476 Salt and hypertension 477 Key facts 477 Overview 477 Historical importance of salt 477 The problems with salt 478 Requirement for salt 479 Amount and sources of dietary salt 480 A review of the evidence for a salt–hypertension link 482 Observational evidence 482 Experimental studies 484 Relationship between salt intake and morbidity and mortality 485 Other factors involved in the aetiology of hypertension 486 Conclusions 487 Key references 488 PART 4 VARIATION IN NUTRITIONAL REQUIREMENTS AND PRIORITIES 491 17 Nutrition and the human lifecycle 493 Introduction 493 Nutritional aspects of pregnancy 495 Pregnancy overview 495 Effects of malnutrition in pregnancy 495 The scale of increased nutritional needs in pregnancy 495 RNI and RDA for pregnancy 496 Pregnancy outcomes 497 Estimating the extra nutritional needs of pregnancy 498 Preconception 498 Energy aspects of pregnancy 499 Protein in pregnancy 502 Minerals in pregnancy 503 Calcium 503 Iron 504 Folic acid/folate and NTDs 505 Other vitamins in pregnancy 505 Alcohol and pregnancy 506 Lactation 506 Infancy 507 Breastfeeding versus bottle-feeding 507 Prevalence of breastfeeding 508 Factors influencing choice of infant feeding method 510 The benefits of breastfeeding 513 Weaning 517 When to wean? 517 What are weaning foods? 518
- 25. xx Contents The priorities for weaning foods 518 Childhood and adolescence 520 Data from the rolling NDNS programme 521 The elderly 525 Demographic and social trends 525 The effects of ageing 527 Nutritional requirements of the elderly 529 The diets and nutritional status of elderly people 531 Energy and macronutrients 531 Levels of overweight, obesity and other risk factors 533 Diet and disease risk in the elderly 535 Key references 538 18 Nutrition as treatment 541 Diet as a complete therapy 541 Overview and general principles 541 Food allergy (including coeliac disease) 542 Immediate hypersensitivity reactions 542 Coeliac disease (gluten-induced enteropathy) 543 Phenylketonuria 545 Diet as a specific component of therapy 546 Diabetes mellitus 546 Classification and aetiology 546 Diagnosis 547 Symptoms and long term complications 547 Principles of management 548 Can type-2 diabetes be reversed? 549 Cystic fibrosis 551 Chronic renal failure 553 Malnutrition in hospital patients 554 Overview 554 Prevalence of hospital malnutrition 555 Consequences of hospital malnutrition 555 The traditional causes of hospital malnutrition 557 Improving the nutritional care of hospital patients 560 Aims of dietetic management of general hospital patients 560 Aids to meeting nutritional needs 560 Measures that could improve the nutritional status of hospital patients 561 Impact of nutritional support 562 The Malnutrition Universal Screening Tool 563 NICE quality standards and guidelines 563 Key references 564 19 Some other groups and circumstances 567 Vegetarianism 567 Introduction 567 Prevalence of vegetarianism 568 The risks and benefits of vegetarian and vegan diets 569 Adequacy of vegetarian diets 569 Vegetarian diets and nutritional guidelines 573
- 26. xxi Contents Racial minorities 574 Introduction and overview 574 The health and nutrition of particular minority groups 575 Dietary comparison of ethnic groups in Britain 577 Nutrition and physical activity 580 Fitness 580 Guidelines 582 Current levels of physical activity and fitness 582 Long-term health benefits of physical activity 585 Introduction 585 Diet as a means to improving physical performance 587 Key references 590 PART 5 FOOD SAFETY AND QUALITY 593 20 The safety and quality of food 595 Aims of the chapter 595 Consumer protection 595 Food law 595 Food labelling 597 Labelling in the UK 597 Labels in the US 598 An overview of health claims 599 Food poisoning and the microbiological safety of food 601 Introduction 601 The causes of food-borne diseases 602 The causative organisms 602 How bacteria make us ill 603 Circumstances that lead to food-borne illness 603 Principles of safe food preparation 606 Requirements for bacterial growth 606 Some specific causes of food poisoning outbreaks 607 Some practical guidelines to avoid food poisoning 608 Minimise the risks of bacterial contamination of food 608 Maximise killing of bacteria during home preparation of food 609 Minimise the time that food is stored under conditions that permit bacterial multiplication 609 A note about treatment of food-borne disease 610 Pinpointing the cause of a food poisoning outbreak 610 A review of some common food poisoning organisms and foodborne illnesses 612 The Campylobacter 612 Salmonella 612 C. perfringens 613 E. coli 0157 and the VTEC bacteria 613 S. aureus 613 B. cereus 614 C. botulinum 614 L. monocytogenes 614
- 27. xxii Contents Bovine spongiform encephalopathy (BSE) 615 Overview 615 The nature of prion diseases 616 The infective agent 616 Causes of prion disease 616 The cattle epidemic of BSE 617 Time course of the epidemic 617 What caused the cattle epidemic? 617 Measures taken to limit vCJD and eliminate BSE 617 The human vCJD epidemic 618 The costs of this crisis 619 Food processing 620 Some general pros and cons of food processing 620 Specific processing methods 622 Canning 622 Pasteurisation 622 Ultra-high temperature treatment 622 Cook chill processing 622 Food irradiation 623 The chemical safety of food 625 Overview of chemical hazards in food 625 Natural toxicants and contaminants 625 Circumstances that may increase chemical hazard 625 Some natural toxicants in “Western” diets 626 Residues of agricultural chemicals 627 Food additives 629 Uses 629 Some arguments against the use of food additives 629 Some counter-arguments 629 Food additive regulation 630 Testing the safety of food additives 631 Key references 634 Index 635
- 28. xxiii Preface The main aims of this book have remained constant over its five editions; I have tried to write a compre- hensive introduction to nutrition that is accessible to a wide range of students, including those with limited mathematical and biochemical background. Whilst not ignoring the nutritional problems of developing countries, the main focus is upon nutritional issues and problems that are considered important in indus- trialised countries like the UK and the USA. As the main market for the book is the UK, recommenda- tions and data from the UK have been central to most discussions, but in many places I have used US data and recommendations to highlight the similarities or sometimes the differences between two affluent industrialised countries. For some topics, I have used data from other sources, especially the WHO, to give a worldwide perspective. For example, I have given past and present rates of obesity and overweight in adults and children in different countries to illustrate how rates have been rising not only in industrialised countries but rising even faster in some developing countries. As another example I have also compared breastfeeding rates around the world; the UK has the world’s worst record for mothers who wholly breast- feed their babies for the recommended 6 months. For the second edition, I introduced bullet point summaries at the end of every section and these have been retained because they are popular with student readers. For some sections, readers might even find it useful to read the summary before reading the main text section. I am now an active blogger (http s://d rgeof fnutr ition.wordpress.com/) and regularly post articles/ essays about aspects of diet, lifestyle and health or make comments about “new research findings” that have generated headlines in the general media. I have also posted many articles about aspects of the methods and processes used in biomedical research and about research fraud. A number of these blog article topics are also discussed in this book. Readers may find the fully referenced blog articles to be a useful extra resource for more in-depth coverage of some of these topics; especially as most have URL links to key sources. What changes have I made to this edition? Although it has been largely re-written, the theme of Chapter 1 is still changing priorities in nutrition edu- cation and research. The traditional priority in nutri- tion was ensuring adequate intakes of energy and all essential nutrients. More recently, an additional aim has been to guide consumers towards a diet that maximises long-term health and reduces morbidity and mortality from the so-called “diseases of indus- trialisation” like heart disease, many cancers, type-2 diabetes, osteoporosis, dental caries and dementia. These expanding aims are reflected in new consumer guides and I briefly review changes in these food guide tools from simple food groups to more elabo- rate food guide plates and pyramids. I end Chapter 1 with a critical discussion of the direction of much recent nutrition research that is focused upon trying to find tenuous links between individual foods or dietary components and the risk of specific diseases. The epidemiological methods used to try to estab- lish such subtle links between diet and diseases are necessarily too crude to identify these links with any degree of confidence. A claim of a weak link based upon this crude methodology can lead to decades of unproductive research which has negligible chance of leading to any clear answer or useful dietary rec- ommendation as exemplified in the yoghurt and ovarian cancer case-study at the end of the chapter. Another stream of current research is an avalanche of papers confirming already well-established links with different data sources and/or ever larger sample sizes such as the association between high fruit and vegetable consumption and reduced mortality that has been almost universally accepted for over 30 years; the methods used cannot establish cause and effect definitively, so a strong association remains
- 29. xxiv Preface an association no matter how large the sample size, detailed the database or sophisticated the statistical manipulations. Chapter 2 deals with the social, cultural and eco- nomic influences upon diet and food selection. I have tried to streamline this chapter whilst still discuss- ing the major topics discussed in earlier editions. A large part of this chapter uses my “hierarchy of avail- abilities” model of food selection as the framework for discussing the many non-nutritional factors that influence food choices. This simple model was based upon the concepts in Abraham Maslow’s famous hierarchy of human needs. Methods of nutritional surveillance and research remain an important part of the book. Chapter 3 dis- cusses methods used to assess nutrient intake and nutritional status. It has been updated. This chapter now includes a discussion of convincing evidence that most methods used to assess nutrient intakes that involve self-reporting substantially under- estimate energy and food intake; this finding has important and far-reaching implications for nutri- tion surveillance and research. The section dealing with the epidemiological and experimental meth- ods used by nutritionists has been fully revised and expanded and is now split into two chapters (4 and 5). Chapter 4 deals with the individual methods and their strengths and limitations. Chapter 5 is about how information from these diverse studies is syn- thesised, amalgamated and translated into practi- cal treatments or recommendations. This chapter also contains a discussion of why many scientists think that many published research findings are not reproducible and probably wrong. These criticisms of current research may apply particularly to nutrition research which relies so heavily upon observational methods. At the end of Chapter 5, there is also a brief discussion of research fraud and some of the cases that have impacted upon nutrition. The methods dis- cussed in Chapters 4 and 5 are used for all biomedi- cal research so some appreciation of these methods should enable students to make a more realistic appraisal of the claims about scientific breakthroughs and particularly links between diet, lifestyle and dis- ease that frequently appear as extravagant headline claims in the popular media. Chapter 6 reviews dietary guidelines and rec- ommendations set by government agencies and the WHO. Despite differences of emphasis and different nuances, these recommendations are consistent and have not changed much over the last three or four decades. There is also a detailed critical review of the current UK recommendations about alcohol use and the new law in Scotland that sets a minimum price for alcoholic drinks. The chapter on cellular energetics and metabo- lism that was present in all previous editions has been removed but some of the content appears in other chapters e.g. the metabolism of fatty acids (β-oxidation) is now moved to the fat chapter. Chapters 7–9 cover energy aspects of nutrition, including, adaptations to starvation; the regulation of energy balance; and the prevalence, causes, con- sequences and treatment of obesity. There is a short critical discussion of the briefly popular notion that a defect in brown fat thermogenesis might be a major cause of human obesity; premature application of data with small mammals played a part in generating this now generally discredited theory. Obesity and associated medical problems like type-2 diabetes has long been a major public health problem in industri- alised countries but is now rapidly becoming a major problem in many parts of the developing world. Chapters 10–16 contain an updated discussion of individual macronutrients (carbohydrate, protein and fat) and micronutrients (vitamins and miner- als). Chapter 10 (carbohydrates) includes discussion of the glycaemic index and of the new UK “sugar tax” on sugary soft drinks. In Chapter 12 (fat) there is an extended discussion of statins and impact their mass use has had upon the blood lipid profile of UK adults and cardiovascular disease risk. Chapter 13 is about dietary supplements and food fortifica- tion. Supplements are classified and the rationale for their use and evidence of their efficacy is evaluated. The case for fortification of UK flour with folic acid and perhaps vitamin D is discussed along with an overview of UK food fortification policy and how it might be modernised. The overall message from this chapter is that many supplements are unnecessary or inherently ineffective. Even where increased intake of a supplement might be beneficial to some people, over-the-counter supplements are a very inefficient means of effecting increasing intakes in those likely to benefit from them. Chapter 14 is a new chapter which brings together material about functional
- 30. xxv Preface foods, so-called “superfoods”, and the benefits of eating large amounts of fruits and vegetables. The term “superfood” is now widely used but the impli- cation that these foods can have a transformative effect upon the diet or health is seriously flawed and naïve; the evidence supporting most specific claims for health benefits of individual “superfoods” is weak or non-existent. Chapters 15 (on vitamins) and 16 (on minerals) remain structurally unaltered from the fourth edition. Chapter 15 begins with an over- view of vitamins and vitamin deficiency followed by a discussion of each individual vitamin. Chapter 16 begins with brief reviews of nine individual minerals followed by a more in-depth discussion of four min- eral-related issues: iodine deficiency; iron and iron deficiency anaemia; calcium, diet and bone health; and the relationship between salt intake and blood pressure. Chapters 17–19 cover nutritional needs and pri- orities of different lifecycle and racial groups, the role of nutrition in disease treatment, vegetarianism and the interaction between nutrition and physical activity. These chapters have been updated and re- worked but remain structurally unaltered. The sec- tion on vegetarianism has been expanded to reflect the implications of increased numbers choosing a vegetarian or partly vegetarian diet in the UK. There has been an increase in people who identify as vegan and increased use and availability of vegetarian alternatives to milk and dairy products. Chapter 20 deals with the safety and quality of food and it is shorter than in previous editions mainly because the sections dealing with functional foods and “superfoods” have been moved to Chapter 14. I contemplated leaving out the section dealing with the bovine spongiform encephalopathy or “mad cow disease” because the crisis seems to be over. However, in the end, I revised it and left it in because it had such profound economic, political and social impact in the UK; it has left a lingering mistrust of government’s ability or willingness to ensure that our food is safe. A NOTE ABOUT REFERENCING When writing a scientific review article, a major aim of the reference list is to show the provenance of statements made in the text and to give the reader an indication of the confidence they should have in any statement or claim; directing readers towards supplementary sources is often very much a sec- ondary aim. In this edition, I have made directing students towards useful supplementary material a more prominent aim of the reference list. A stream- lined list of key references is now given at the end of each chapter rather than a long list of references at the end of the book or only available as an online resource as in the fourth edition. I have tried to minimise references given just as support for state- ments made, especially long-accepted statements, and to maximise those that some interested readers might actually choose to look up. I have also tried, where possible, to list references that are acces- sible online and to minimise, for example, refer- ences to out-of-print or difficult to obtain books or book chapters. Where a discussion in the text has been covered in one of my blog articles, I give the listed blog address in the references but not the individual sources cited as these can all be accessed from the blog article. I have cited many Cochrane reviews and these are available free online to read- ers in most countries from the searchable Cochrane Database of Systematic Reviews (http s://w ww.co chranelibrary.com/cdsr/reviews). I have not given the full citation for each of these in the reference list but readers are given enough information in the text to find these using the search facility of the database; this will also find the latest update of the review.
- 32. xxvii Acknowledgement I would like to thank my commissioning editor at Taylor and Francis Ms Randy Brehm. Her persis- tence and encouragement eventually persuaded me to write this fifth edition even though she is based in Florida, several thousand miles away from me in London.
- 34. xxix About the author Geoffrey P. Webb, BSc, MSc, PhD, SFHEA, has a BSc in physiology and biochemistry and a PhD from University of Southampton and an MSc (dis- tinction) in Nutrition from King’s College, London. He has many years’ experience of teaching nutri- tion, physiology and biochemistry at the University of East London and is a senior fellow of the Higher Education Academy. Early in his career he led an obesity research group and published results which questioned the once-fashionable notion that a defect in brown fat might be an important cause of human obesity. In recent years, he has focused his efforts on writing books and review articles, and several of his reviews have related to the discussion of major scientific errors and critical discussion of the research methods used in nutrition and public health research. This fifth edition is his tenth book i.e. ten editions spread over four different titles. Three of his books have been translated into Spanish and one into Polish. He also wrote a monthly “nutrition and health” column for a local East London newspaper for three years and regularly blogs about nutrition, public health, research methods and research fraud. He served as a member of the editorial board of the British Journal of Nutrition for about 8 years. He has spent several years researching many cases of research fraud and is in the process of draft- ing a new book about error and fraud in biological and medical research.
- 36. PART 1 CONCEPTS AND PRINCIPLES 1 Changing priorities in nutrition 3 2 Food selection 19 3 Methods of nutritional assessment and surveillance 47 4 Investigating links between diet and health outcomes 89 5 Investigating links between diet and health – amalgamation, synthesis and decision making 117 6 Dietary guidelines and recommendations 141
- 38. 3 1 Changing priorities in nutrition ENSURING ADEQUACY AND USE OF FOOD GROUPS During the first half of the twentieth century, the focus of nutrition research was to identify the essen- tial nutrients and to quantify our requirements for these nutrients. Essential nutrients are split into two major categories. • The macronutrients – carbohydrates, fats and protein are required in relatively large quantities and are the main sources of dietary energy. Within the fats category, small amounts of certain polyunsaturated fatty acids are specifically essential and needed for vitamin-like functions; one of them was originally designated vitamin F. Within the protein component, nine or ten amino acids are termed essential because they are needed for protein synthesis and cannot be made from the other 10/11 so-called non-essential amino acids; some are also needed in other synthetic pathways. We can synthesise glucose from some amino acids and from the glycerol component of fat, but in most healthy diets, carbohydrates would be expected to provide more than half of the calories. • The micronutrients – vitamins and minerals are only required in small (milligram or microgram) quantities and do not act as sources of energy. There are 13 vitamins and 15 unequivocally established essential minerals. The following list gives the criteria for establishing that a nutrient is essential. • The substance is essential for growth, health and survival. • Characteristic signs of deficiency result from inadequate intakes and these are only cured by administration of the nutrient or a specific precursor. • The severity of the deficiency symptoms is dose-dependent; they get worse as the intake of nutrient decreases. • The substance is not synthesised in the body, or only synthesised from a specific dietary precursor, and so is required throughout life. Ensuring adequacy and use of food groups 3 A new priority – reducing the chronic diseases of ageing populations 6 Plates and pyramids: food guides to reflect modern nutritional priorities 7 Failure to fully implement better nutritional knowledge and understanding 9 The future of nutrition research 12 Yoghurt and ovarian cancer? A case study of unproductive research 14 Key reference 17
- 39. 4 Changing priorities in nutrition Note that a strict application of this rule would eliminate vitamin D, which can be synthesised in the skin in sufficient amounts by a photochemical reaction, provided it is regularly exposed to summer sunlight. During the first half of the twentieth century, most of these essential nutrients were identified and their ability to cure or prevent certain deficiency diseases was confirmed. These deficiency diseases have been major causes of ill-health and mortality and in a few cases still are. • Between 1900 and 1950 there were 3 million cases and 100,000 deaths from pellagra in the USA, a disease that was shown to be caused by a lack of niacin or vitamin B3. It has been a major cause of ill-health in many places where maize was the dominant staple food. • In the early 1900s, there were 30,000 deaths per year from beriberi in British Malaya and up to 20,000 in the American-occupied Philippines. Beriberi was shown to be caused by a lack of thiamin (vitamin B1) and was prominent in other countries where white (polished) rice was the dominant source of dietary calories. • In the late nineteenth and early twentieth centuries, up to 75% of children in some British industrial cities and some northern US cities like Boston suffered from rickets caused by vitamin D deficiency. Inadequate exposure of the skin to summer sunlight was the major underlying cause. • Prior to the 1920s, a diagnosis of pernicious anaemia meant death was almost inevitable until it was found that eating raw liver (a very rich source of vitamin B12) could alleviate this condition. The condition is caused by an inability to absorb vitamin B12. The impact of this work was such that several Nobel Prizes for Physiology or Medicine and for Chemistry were awarded for vitamin-related work; between 1929 and 1943 a total of 14 individuals shared seven Nobel prizes for such work. In most cases, these nutrients have not only been identified but firm estimates of average requirements have also been made. Selenium was the last of the 28 micronutrients to have its essentiality established in 1957. Many governments and international agencies use these estimates of requirements to publish lists of dietary standards that can act as yardsticks to test the adequacy of diets or food supplies. These stan- dards are variously termed Recommended Dietary/ Daily Allowances (RDA) or Dietary Reference Values (DRV) and they are discussed fully in Chapter 3. During these early decades of the twentieth cen- tury, our understanding of the nature, roles and requirements for essential nutrients was established and ensuring adequacy became the overriding prior- ity in nutrition. Good nutrition was all about making sure that people got enough energy and protein and adequate amounts of all of the essential nutrients. The quality of a diet would have been judged upon its ability to supply all of the essential nutrients and to prevent nutritional inadequacy. The official priorities for improving the nutri- tional health of the British population during the 1930s were the following: • To reduce the consumption of bread and starchy foods. • To increase the consumption of nutrient-rich, so-called “protective foods”, like milk, butter, cheese, eggs, fruit and green vegetables. The following benefits were expected to result from these changes: • A taller, more active and mentally alert population. • Less of the deficiency diseases like goitre, rickets and anaemia. • A reduced toll of death and incapacity due to infectious diseases like pneumonia, tuberculosis and rheumatic fever. These aims have largely been achieved. The aver- age height of Britons has increased and they are now much taller now than in the first half of the twentieth century. Occurrences of overt deficiency diseases are now rare and usually confined to particular high- risk sectors of the population like those with chronic illnesses or those at the extremes of social and eco- nomic deprivation. Children now mature faster and reach puberty earlier. The potential physical capa- bility of the population has undoubtedly increased even though many of us are unfit because we are not required to do any hard physical work and can
- 40. 5 Ensuring adequacy and use of food groups choose to lead very inactive lives. Infectious diseases now account for less than 1% of deaths in Britain. There are still many populations around the world where people struggle to obtain enough food to eat and where malnutrition and certain deficiency dis- eases are still prevalent; ensuring dietary adequacy remains the nutritional priority for such populations. Even within affluent countries, those at the extremes of social and economic deprivation may still strug- gle to achieve sufficient dietary adequacy to pre- vent overt indications of deficiency or malnutrition. Prolonged periods of ill-health may also precipitate malnutrition. Many people in the UK without vis- ible symptoms of deficiency still have intakes of vita- mins and minerals that are considered inadequate and/or have biochemical indicators that are below the threshold values taken to indicate poor status for particular nutrients. Right up until the 1990s the guidance tools used by those seeking to give public health advice about diet and nutrition reflected this prioritising of ade- quacy. Foods were grouped according to their abil- ity to supply important elements of an adequate diet and clients advised to eat food from each of these groups each day. A food chart poster produced by the Ministry of Food in Britain during World War II (WW2) splits foods up into four groups and recom- mends that people “eat something from each group every day”. The four groups used were: • Body-building foods – these were all high protein, animal foods: milk, meat, eggs, cheese and fish. In a footnote it is acknowledged that many vegetable foods like peas, beans, bread and potatoes help in body-building but are not as good as the five listed. • Energy foods – a list of 17 quite disparate foods: starchy foods including potatoes, bread, oatmeal and rice; sugar and other sugary foods like honey and dried fruit; foods with a high fat content like butter, margarine, several fatty meats and dripping (fat that has dripped from roasting meat usually beef). • Protective foods, group 3 – this is a list of foods likely to contain fat-soluble vitamins like the oily fish herring and salmon, liver, eggs, dairy foods, margarine, butter and other dairy foods (fortification of margarine with vitamins A and D began during WW2). • Protective foods, group 4 – this is a list of seven foods likely to contain carotene (vitamin A), water-soluble vitamins and minerals: potatoes, carrots, fruit and green vegetables, salads, tomatoes and wholemeal/brown bread (fortification of white flour also began during WW2). Some of the suggestions in this poster seem rather odd in the context of modern recommendations which favour low (saturated) fat and low sugar diets with high intakes of fruit, vegetables and unrefined cereals but only modest amounts of dairy foods and meat. The classification of butter and margarine as protective foods and the positive presentation of sugar as an energy food may strike a particularly dis- cordant note with modern nutritionists whose focus is on excessive energy intake and the major public health problems caused by obesity. A much more familiar food grouping system is the Four Food Group Plan, which was the mainstay of dietary guidelines for around four decades, espe- cially in the USA. This plan uses four groups and rec- ommends minimum numbers of portions from each group each day. These four groups and their essen- tial nutrient profiles are outlined in the following list, along with minimum portion recommendations. • The milk group – milk, cheese, yoghurt, other milk products and would now include vegetarian dairy alternatives like soya milk and other non-dairy “milks” and alternatives to dairy products that can be made from them. These provide good amounts of energy, high- quality protein, vitamin A, calcium, iodine and riboflavin. At least two portions each day. • The meat group – meat, fish, eggs and vegetarian alternatives to meat like pulses, soy protein, nuts and more recently Quorn. This group provides protein, B vitamins, vitamin A, iodine and iron. At least two portions per day. • The fruit and vegetable group – fruits and vegetables, and pulses other than those included in the meat group. Seen as good sources of carotene (vitamin A), vitamin C, folate, riboflavin, potassium and fibre. At least four portions per day.
- 41. 6 Changing priorities in nutrition • The bread and cereals group – bread, rice, pasta, breakfast cereals, other cereals and products made from flour. Whole grain cereals were seen as good sources of B vitamins, some minerals and fibre. In the UK (and the USA) white flour and many breakfast cereals are fortified. At least four portions per day. Even though there are differences between these two grouping systems, the common theme of both of them is the emphasis upon adequacy, making sure that people get enough energy, high-quality protein, vitamins and minerals epitomised by the phrase “at least 2/4 portions per day” in the four food group plan. A NEW PRIORITY – REDUCING THE CHRONIC DISEASES OF AGEING POPULATIONS In 1901, the average life expectancy was around 47 years in both Britain and the USA. It is now well over 75 years in both countries. In 1901, less than half of British people survived to reach 65 years but now it is around 95%. In 1901, only 4% of the population of Britain was over 65 years but now they make up 16% of the population. These dramatic increases in life expectancy have been largely the result of reducing deaths from acute causes like infection, complica- tions of childbirth, injury and appendicitis, especially among children and younger adults. Life expec- tancy has increased substantially for all age groups, including the elderly, over this period. This inevita- bly means that there have been big increases in the proportion of deaths attributable to the chronic, degenerative diseases of affluence/industrialisation that affect mainly middle-aged and elderly people. Infectious diseases were the major cause of death in Britain in the nineteenth century but now the cardio- vascular diseases (heart disease and strokes), cancers and increasingly dementia account for the majority of deaths in the UK. Infectious diseases accounted for 1 in 3 deaths in Britain in 1850, and about 1 in 5 deaths in 1900, but today this figure is under 1%. At the turn of the twentieth century probably less than a quarter of all deaths were attributed to all cardio- vascular diseases, strokes and cancers but now it is three quarters. In the period 1931–1991, cardiovas- cular diseases rose from causing 26% of all deaths to 46% although death rates from heart disease have seen a very substantial drop since then, and since the start of the new millennium have just about halved in UK men. These diseases of industrialisation were shown to be associated with a sedentary lifestyle and diets that are high in (saturated) fat, sugar and salt but relatively low in starch, dietary fibre and fruits and vegetables. Many sets of guidelines published by government agencies since the late 1970s have focused upon dietary changes intended to reduce the toll of these chronic degenerative diseases, which particularly afflict ageing populations (see Chapter 6 for discussion of these different sets of guidelines). The consensus of these reports and numerous sub- sequent ones for industrialised populations are sum- marised in the list that follows. • Maintain body weight within the ideal range and avoid excessive weight gain by restricting energy intake and/or increasing energy expenditure (exercise). • Eat a varied diet. • Eat plenty of starchy and fibre-rich foods; starch should be 40% or more of the total food energy with at least 25–30 g/day of dietary fibre. • Eat plenty of fruits and vegetables: at least five portions per day. • Eat two portions of (oily) fish per week. • Moderate the proportion of fat and saturated fat in the diet; less than 35% or even less than 30% of food energy should come from fat with no more than around 10% from saturated fatty acids. • Reduce salt consumption to 5 or 6 g/day. • Reduce added sugars to 5–10% of energy. • Limit the consumption of alcohol to 3 (women) or 4 (men) units per day or even less in more recent UK recommendations. These recommendations have not changed in their main characteristics over the last 40 years. The emphasis in industrialised countries has moved from ensuring that we eat enough energy, protein and nutrients to ensure adequacy to reducing the toll of chronic age-related diseases. This new aim requires reduced intake of certain dietary constituents like
- 42. 7 Plates and pyramids: food guides to reflect modern nutritional priorities fatty meat, full-fat dairy products, sugary or salty foods and some high (saturated) fat products used for cooking or spreading. These latter foods should be replaced by more starchy foods, unsaturated veg- etable oils, low fat spreads, fruits and vegetables. PLATES AND PYRAMIDS: FOOD GUIDES TO REFLECT MODERN NUTRITIONAL PRIORITIES The early food guidance tools based upon food groups and designed primarily to ensure dietary adequacy needed to be modified in order to reflect these new priorities. In 1992 the Food Guide Pyramid shown in Figure 1.1 was adopted as the new food guide tool in the USA. This is a recognisable development of the four food group plan but reflected the new priorities of reducing sugar and fat (especially saturated fat), increasing the starch and fibre content of the diet and increasing the intake of fruits and vegetables. The likely sources of dietary fat and added sugars within the six food groupings are indicated by the density of circles (fat) and triangles (added sugar) within the pyramid’s six compartments. This guide was intended to steer consumers towards a diet that is not only adequate in all the essential nutrients but also reflected these new priorities aimed at reducing or delaying the so-called diseases of industrialisa- tion or affluence. A food guide in the form of a tilted plate was introduced in the UK in 1994 with essentially the same aims and it was similarly a recognisable development of the old four food group plan (see Figure 1.2). These food guides have been updated and modi- fied since 1992. Figure 1.3 shows the latest Eatwell Milk, Yogurt Cheese Group 2-3 SERVINGS Meat, Poultry, Fish, Dry Beans, Eggs Nuts Group 2-3 SERVINGS KEY Fat (naturally occurring and added) Sugars (added) These symbols show fats and added sugars in foods. Fruit Group 2-4 SERVINGS Bread, Cereal, Rice Pasta Group 6-11 SERVINGS Vegetable Group 3-5 SERVINGS Fats, Oils Sweets USE SPARINGLY Figure 1.1 The Food Guide Pyramid introduced in the USA in 1992.
- 43. 8 Changing priorities in nutrition Guide published in 2016 by Public Health England. The oils and spreading fats sector in the new plate is now very small and foods like potato crisps (chips), bottled sauces, biscuits, cakes, candies and choco- late are outside the plate altogether and consumers are advised to consume these less often in smaller amounts. Around the outside of the plate are a series of message linked to the four food groups like choos- ing options that are lower in fat, high fibre or without added sugar. There is advice about consuming six to eight portions of fluids each day but to mainly choose water, low-fat milk, sugar-free options as well as tea and coffee. There is advice to limit fruit juices to around 150 ml/day. Finally, consumers are advised to make use of the “traffic light” labelling on foods (see Chapter 20). The 1992 Food Guide Pyramid in the USA was replaced with a new MyPyramid image in 2005 (see Figure 1.4). This changes the layout of the pyramid which is now divided vertically rather than horizon- tally, but the message remains essentially unaltered from 1992. The one additional feature is a figure climbing steps on the side of the pyramid to encour- age consumers to be active and to balance calorie intake with output. Whilst the images and emphasis have evolved in these food selection guides, the general dietary characteristics being encouraged have not changed in their overall aims. This means that for more than 40 years we have had a pretty good idea of what nutrients are essential, how much of these are needed to prevent any indications of deficiency and the general characteristics of a diet that would reduce or delay the toll taken by the diseases of affluence/ industrialisation. In the most recent US food guide there is yet another change of format and as in the UK, the image of a plate is used (see Figure 1.5). The plate in this image is divided into four similar-sized sectors labelled fruits, vegetables, grains and protein with a glass/cup by the side of the plate labelled dairy. The plate is accompanied by ten tips with accompanying explanation and examples for building a healthy eat- ing style for life: Meat, fish and alternatives Foods containing fat Foods and drinks containing sugar There are five main groups of valuable foods Milk and dairy foods Bread, other cereals and potatoes Fruit and vegetables The Balance of Good Health Figure 1.2 The UK food guide plate of 1994.
- 44. 9 Failure to fully implement better nutritional knowledge and understanding • Find your own healthy eating style. • Make half your plate fruits and vegetables. • Focus on whole fruits. • Vary your veggies. • Make half of your grains whole grains. • Move to low-fat or fat-free milk or yoghurt. • Vary your protein routine (from a listed range of seafood, beans and peas, unsalted nuts and seeds, soy products, eggs, lean meats and poultry). • Drink and eat beverages and foods with less sodium, saturated fat and added sugars. • Drink water instead of sugary drinks. • Everything you eat and drink matters. Consumers are effectively being given general guidelines that they should use to develop a life- long healthy eating plan that suits them. This lat- est US guide is almost reverting to the past idea of food groups plus additional advice on how to select healthy options within those food groups. FAILURE TO FULLY IMPLEMENT BETTER NUTRITIONAL KNOWLEDGE AND UNDERSTANDING This long-standing improvement in the breadth and depth of knowledge and understanding of nutri- tion has not always been fully translated into health improvement. • In 1915, David Marine said that “endemic goitre is the easiest known disease to cure” yet hundreds of millions still suffer from goitre or other manifestations of dietary iodine deficiency and this is still the most common, preventable cause of mental retardation in the world’s children. • Hundreds of thousands of children in the world still die or go blind each year due to vitamin A deficiency (“factor A”extracted from butter fat c1914). Check the label on packaged foods Each serving (150g) contains Use the Eatwell Guide to help you get a balance of healthier and more sustainable food. It shows how much of what you eat overall should come from each food group. Eatwell Guide Choose foods lower in fat, salt and sugars Eat less often and in small amounts 6-8 a day Water, lower fat milk, sugar-free drinks including tea and coffee all count. Limit fruit juice and/or smoothies to a total of 150ml a day. Choose unsaturated oils and use in small amounts Oil spreads of an adult’s reference intake Typical values (as sold) per 100g: 697kJ/ 167kcal Per day 2000kcal 2500kcal = ALL FOOD + ALL DRINKS Sugars 34g Salt 0.9g 7% Saturates 1.3g Energy 1046kJ 250kcal Fat 3.0g 13% 4% LOW LOW 38% HIGH 15% MED E a t a t l e a s t 5 p o r t i o n s o f a v a r i e t y o f f r u i t a n d v e g e tables every day Eat more beans and pulses, 2 portions of which is oily. Eat less and processed meat sustainably sources fish per week, one of Choose lower fat and lower sugar options Choose w h o l e g r a i n o r h i g h e r f i b r e v e r s i o n s w i t h l e s s a d d e d f a t , s a l t s u g a r F r u i t a n d v e g e t a b l es Beans, pulses, fish, eggs, meat and other proteins Pota t o e s , b r e a d , r i c e , p a s t a a n d o t h e r s t a r c h y c a r b o h y d r a t e s Dairy and alternatives Figure 1.3 The Eatwell Guide, the latest (2016) development of the UK Food Guide.
- 45. 10 Changing priorities in nutrition GRAINS VEGETABLES FRUITS MILK MEAT BEANS Figure 1.4 The 2005 US MyPyramid food guide. Vegetables Fruits Grains Protein Dairy Figure 1.5 The new American MyPlate food guide.
- 46. 11 Failure to fully implement better nutritional knowledge and understanding This failure to fully realise the benefits of better nutrition knowledge is not confined to developing countries. In the UK many people have intakes of an essential vitamin or mineral that are classified as inadequate i.e. more than two standard deviations below the estimated average requirement (termed the lower reference nutrient intake [LRNI] in the UK). There are also many people who have bio- chemical indicators of nutrient status that are below the minimum thresholds used to indicate adequacy. • According to a major UK report on iron and health, over half of institutionalised elderly people had blood haemoglobin levels indicative of iron deficiency anaemia, and even in the free-living elderly, anaemia rates ranged from 6% of women aged 65–74 years to 38% of men aged over 85 years (anaemia rates are higher in men than women in the elderly). The same report found that 9% of adolescent girls were anaemic, 24% had depleted iron stores (low serum ferritin) and 48% had total iron intakes below the LRNI (see Chapter 16). • In 2012–2013 there were well over 800 admissions of children to British hospital for rickets (vitamin D deficiency) and during the winter months well over 30% of UK adults are below the biochemical threshold indicative of vitamin D inadequacy; double this number if the higher threshold used by the American Institute of Medicine is used (see Chapter 15). • Many British women and girls have inadequate iodine intake; perhaps half of teenaged girls have urinary iodine concentrations indicative of at least mild iodine deficiency There is preliminary evidence that poor iodine status of pregnant UK women is adversely affecting the intellectual development of their offspring (see Chapter 17). Clear evidence has existed since 1991 that daily sup- plements (400 µg) of folic acid (vitamin B9) taken from before conception and in early pregnancy reduce the incidence of neural tube defects, like anencephaly and spinal bifida, in babies by around three quarters. Yet advising women to take over-the-counter sup- plements when planning a pregnancy has had little impact on the rates of neural tube defects. In 1998, the US and Canadian authorities introduced manda- tory fortification of flour with folic acid and this led to immediate and substantial falls in the incidence of these neural tube defects. Over eighty countries have followed this North American lead but despite repeated recommendations from expert bodies, UK and other European governments have resisted introducing similar measures and this has resulted in thousands of avoidable stillbirths, infant deaths, terminations and births of severely disabled babies (see Chapter 13). The first British report to set quantitative targets for dietary changes that would reduce the risks of chronic degenerative disease (the National Advisory Committee for Nutrition Education [NACNE] report) was produced in 1983. It set some targets that it envisaged could be achieved within 5 years, i.e. by 1988, and also more ambitious targets that might take 15 years to be reached, i.e. by 1998. It set a 5-year target for reducing the proportion of dietary energy that should come from fat to no more than 35%. This target re-appeared in the Department of Health’s Health of the Nation report as a target for 2005, and data from National Diet and Nutrition Survey sug- gest that this preliminary NACNE target may actu- ally have been reached in around 2010 i.e. more than 20 years later than envisaged by NACNE. In 1990 the WHO made a recommendation that we should eat 5×80 g portions of fruit and vegetables each day and this resulted in campaigns to promote 5 a day in sev- eral countries, including the UK (in 2003). Despite these WHO recommendations being made over 25 years ago and an active 5 a day campaign in the UK since 2003, most British adults are still eating less than 3 portions per day. In about 15 years the 5 a day campaign has had only a small impact on the average consumption of fruit and vegetables. The examples in the previous paragraph suggest that major improvements in nutritional health in both industrialised and developing countries are not now being held back primarily by a lack of scientific knowledge and understanding but by economic and political factors and a lack of compliance with nutri- tional advice and guidelines. Major and relatively costly vaccination and pub- lic health programmes have had a major worldwide impact in reducing the toll of some diseases. Such
- 47. 12 Changing priorities in nutrition measures have eradicated smallpox, eliminated polio in all but a handful of countries and greatly reduced the prevalence and deaths from measles; one pro- gramme has even succeeded in eradicating the cattle disease rinderpest. Despite these great public health successes, deficiency diseases that could be cured or prevented by a simple dietary supplement or food fortification like iodisation of salt have not been eradicated. These deficiency diseases still exact an enormous toll of death and disability in many parts of the world even though cheap and effective cures have been known for a century. In affluent industrialised countries, vitamin and mineral supplements or, more probably, selective food fortification could also eradicate adverse con- sequences of deficiency and produce other benefits. Some examples are listed subsequently and more detailed discussion of these issues can be found in other chapters of this book. • Iodisation of salt (including that used by food manufacturers) would eliminate sub-clinical iodine deficiency in Britain which could lead to improvements in child development. • Fortifying flour with folic acid (vitamin B9) would substantially reduce the number of babies in Britain and Europe affected by a neural tube defect and so reduce miscarriages, stillbirths, terminations and children with major lifelong disabilities. It would also largely eliminate folic acid deficiency. • Fortification of a common food with vitamin D would reduce the relatively small number of cases of rickets in the UK as well as reduce the high prevalence of sub-clinical vitamin D deficiency. This would be expected to lead to improved musculoskeletal health of the population and improved immune function; there is evidence varying from fairly convincing to speculative that it might reduce other problems like osteoporosis-related fractures in the elderly and autoimmune diseases like type-1 diabetes and multiple sclerosis (see Chapter 15). • Fluoridation of water supplies up to a level of 1 mg/L would lead to fewer dental caries and immediate improvements in the dental health of UK children and eventually the whole population (see Chapter 10). It is understandable and desirable that governments should be cautious about taking steps like these. Some would argue that it amounts to mass medica- tion without consent, but mandatory fortification of white flour and margarine has been used in the UK and elsewhere since WW2. Voluntary fortification of foods dates back to the 1920s and manufacturers choose to fortify many foods, notably breakfast cere- als, as a marketing aid. There may be ways of allow- ing “freedom of choice” but still ensuring that the extra nutrients reach most of those who would benefit e.g. the UK government could formally recommend folic acid fortification of bread/flour but unfortified products could still be permitted to be sold provided they carry a warning such as “not fortified with folic acid (vitamin B9), an essential nutrient and so does not comply with government recommendations on fortification”. THE FUTURE OF NUTRITION RESEARCH Nutrition research has had an illustrious history stud- ded with many award-winning discoveries capable of transforming and extending the lives of millions of people around the world. The previous discussion also suggests that some of these major discover- ies and developments in nutritional understanding have yet to be fully translated into the concerted and effective measures necessary to realise all of the potential benefits. This area of translation of nutri- tional understanding into practical dietary improve- ments and health benefits seems like a key area for research and resources. This would be of benefit to both developed and developing countries. What are the barriers that prevent sometimes very cheap and simple measures from being widely implemented even many decades after scientific confirmation of their effectiveness? Why does iodine deficiency still affect millions of people around the world and still cause mental retardation in hundreds of thousands of children? Why does vitamin A deficiency still cause blindness, increased infection and increased child mortality in many countries? Why are vitamin and mineral inadequacies and sometimes even an overt deficiency disease like rickets still an issue in some affluent countries despite widespread use of vitamin
- 48. 13 The future of nutrition research and mineral supplements? Why has fruit and veg- etable consumption increased so little in countries like the UK despite decades of campaigns to increase consumption of which most people are aware? Why have European governments been so reluctant dur- ing peacetime to formally recommend or compel the fortification of foods with certain essential nutrients where deficiency is known to be prevalent or where the benefits of supplementation have been proven? Much current nutritional research seems to lack real purpose and direction. This is certainly true of much of the research that is conveyed to the general public in simplistic and sometimes contradictory media headlines. Much of the research that gener- ates headlines in the media is focused on looking for improbable or tenuous links between individual foods or food components and diseases. Some of this research linking dietary components and diseases is improbably presented as having potential for drug discovery. Many important drugs certainly have their origins in plants or other natu- ral products, but when I have asked my pharmacol- ogy colleagues for examples of drugs that have been derived from something with an authentic culinary use, I have received few convincing examples; it is difficult to think of any major drug that has come from a common food. The nature of drug actions means that they are likely to have side effects and to be toxic in excess; many of the potential drugs in plants also have an unpleasant taste or induce unpleasant pharmacological responses. For such reasons this failure of foods to be a useful source of drugs might be expected as we have learnt to avoid eating them. Many papers report that a high or low intake of a food or component is associated with an increased or decreased risk of developing a particular disease or report that studies with isolated cells or animal mod- els give some preliminary evidence for such links. These associations or effects are usually weak and inconsistent and even where statistically significant the effect size is usually small. In many cases there may be a steady trickle of papers, some of which support the association and some which do not. In most of these cases there seems little prospect that evidence will accumulate in the foreseeable future that is strong enough to justify encouraging dietary change based on any one of these claimed links; in many cases, the small measured effects in epidemio- logical studies may simply indicate the degree of bias in the study. It is likely that many such claims will become another research blind alley which will soak up researchers’ time and resources and generate papers for many years, but with no serious prospect of producing any practically useful conclusion. I spent a few minutes searching the BBC news website (http://www.bbc.co.uk/news) and found many headlines making such associations over the last few years or so (see the sample list that follows). Some of them make a fleeting appearance and then disappear whereas others crop up several times. For example: • blackberries and dementia; • olive oil and cancer/inflammation; • green tea and cancer/Alzheimer’s/heart disease/arthritis/HIV/obesity; • garlic and cancer/heart disease/methicillin- resistant Staphylococcus aureus (MRSA)/ malaria; • turmeric and cancer/arthritis/Alzheimer’s disease/cystic fibrosis; • fish oil and depression/anti-social behaviour/ exam performance; • pomegranates and cancer/heart disease; • watercress and cancer; • vitamin C and infections/cancer/blood pressure/gout; • broccoli and cancer/arthritis/heart disease. It seems unlikely that any of these will turn out to make any significant contribution to the preven- tion or treatment of disease or improving health. Probably, their only value will be in their marketing value for some products and boosting the publication credits of the researchers involved. I would also question the value of expensive stud- ies confirming over and over again associations that are already well established with ever larger num- bers of subjects and ever more elaborate statistical analyses (eg the association between high fruit and vegetable intake and reduced cardiovascular mortal- ity). An association between diet and disease still remains just an association even if the study involves many hundreds of thousands or even millions of subjects. Unless a new study is able to make a sig- nificant improvement to the process of identifying,
- 49. 14 Changing priorities in nutrition quantifying and correcting for confounding vari- ables, is it not just confirming what has been gener- ally accepted, in the case of fruit and vegetables, for several decades? Is there too much emphasis on research about dietary nuances that are essentially designed to provide ammunition for effecting more extreme changes or for marketing specific foods to the afflu- ent, worried well rather than improving population health? Should we be agonising over whether 5, 7 or even 10 portions of fruit and vegetables is technically optimal (or which type of fruit or vegetable is best) when 75% of the UK population fails to reach 5 a day and half fail to reach 3 a day? Much of the research on so-called “superfoods” (see Chapter 15) seems to offer little prospect of improving population health and is primarily aimed at marketing specific foods, often new or expensive foods, to affluent, health- conscious people whose diets are already much bet- ter than those of the bulk of the population. In other parts of this book, there are examples of research areas that will probably lead into blind alleys, soak up research effort and resources and contribute to the deluge of unproductive research papers without advancing nutritional understand- ing. Huge amounts of research effort have been devoted to testing the possible disease-preventing or therapeutic value of oily fish or fish oil supplements. Despite many thousands of research studies since the 1970s, there is no substantial evidence that oily fish or fish oil supplements are specifically beneficial in the treatment or prevention of any disease. It has even been suggested that the original trigger for this research, the low rates of heart disease in Eskimos, may have been based upon faulty data (see full dis- cussion in Chapters 12 and 13). Evidence that Brassica vegetables, like broc- coli, might have specific beneficial effects in the prevention or perhaps even the treatment of some cancers has been sought in thousands of papers, yet the National Cancer Institute concluded in 2012 that there is no consistent evidence that eating Brassica vegetables reduces the risk of cancer (see Chapter 14). Much research has been devoted to investigat- ing the cardio-protective effects of drinking alcohol and red wine in particular. Some components of red wine, especially resveratrol, have been promoted as potential panaceas for a range of human ills. This research is underpinned by scores of studies which have reported that when alcohol intake is plotted against mortality in cohort studies then a so-called J-curve is often produced, which signifies that mortality, specifically cardiovascular mortality, falls at low doses but rises as the dose rises. It is now argued that this J-curve is an artefact caused by errors in the correction for other confounding factors and the presence of many ex-drinkers and people with ill-health in the no drinking group (see Chapter 6). There are a number of examples of largely unpro- ductive major research areas, including those men- tioned previously in the chapter, discussed in other chapters of this book. In the last few pages of this chapter there is a case study of how a weak obser- vational link can spawn a large body of unproduc- tive research output that was never likely to produce any finding that would be able to contribute to useful dietary advice. YOGHURT AND OVARIAN CANCER? A CASE STUDY OF UNPRODUCTIVE RESEARCH This case study is a summarised version of an article posted on my blog (Webb, 14 July 2016) and this full article has links to the sources cited). Cramer et al. (1989) published a paper in The Lancet which was widely interpreted as suggesting that high consumption of certain dairy products, notably yoghurt, might increase the risk of ovarian cancer. A UPI press release commenting upon this paper starts with the statement: “A new study suggests that eating large amounts of dairy products, especially yogurt and cottage cheese may increase the risk of developing ovarian cancer…”. The lead author is quoted as saying that he “Stressed the findings need to be confirmed before recommending women eat less dairy products”.
- 50. 15 Yoghurt and ovarian cancer? A case study of unproductive research But “The findings were cause for concern, especially for women who eat a lot of yogurt”. This research was reported in the popular press at the time e.g. the following headline appeared in the New York Times in July 1989: “Research Links Diet and Infertility Factors to Ovarian Cancer”. Cramer and his colleagues were testing the hypothesis that high galactose consumption (from lactose in milk) could promote the development of ovarian cancer. This hypothesis was based upon observations that suggested that high galactose con- centrations might be toxic to the ovarian tissue. For example, women with the rare, hereditary disease galactosemia have impaired ovarian function, fertil- ity problems and premature menopause. This con- dition is characterised by an inability to metabolise galactose and high blood galactose levels. Cramer et al. attempted to compare the consump- tion of dairy products and lactose/galactose in 240 white Boston women recently diagnosed with ovar- ian cancer and a similar number of healthy, white women matched for age and residential district, i.e. a retrospective case-control study (see Chapter 4). They attempted to make a relatively crude estimate of the lactose intakes of the two groups and also a crude categorisation of their consumption of 11 different dairy products. They found no difference between the lactose consumption of the two groups. In about half the subjects, they also measured the activity of an enzyme that metabolises galactose and when they calculated the ratio of galactose concentration to enzyme activity they found a significantly higher ratio in the cancer cases. When they compared the intake of several dairy products in the two groups they found statistical differences for yoghurt and for cottage cheese; cases were 1.7 times more likely to eat yoghurt at least once a month and 1.4 times more likely to eat cottage cheese monthly. There are many flaws in this study that under- mine any conclusion that galactose or any dairy foods cause ovarian cancer. • The dietary classification is necessarily crude and although the aim was to assess diet before diagnosis, it is still quite possible that the recorded intakes were affected by early stages of the disease or the diagnosis. It is notoriously difficult to get a valid and reliable assessment of even the current diets of free-living people. • The two groups were not well matched. The cases were more likely to be Jewish, college educated, never married, never had a child and never used oral contraception. • There was no difference between the two groups in the primary endpoint, and only when multiple analyses were made and a further 12 endpoints compared did they find statistically significant differences. Multiple analysis increases the likelihood of significant differences occurring by chance. Were intakes of any of the other 116 foods in the dietary questionnaire different between the two groups? • The study was necessarily small and underpowered and small studies are again likely to generate false significant effects; the enzyme level was only measured in half the sample. Good, large studies tend to produce effects that are clustered closely around the “true” effect, but as studies get smaller the variability increases, with a greater likelihood of generating some statistically significant results by chance. • The enzyme activity was measured in the cases after diagnosis and treatment. The disease or treatment may have affected enzyme activity or perhaps low enzyme activity is a marker for those who are susceptible to the disease. • The effect size is small and given the crudeness of the methodology and, given the problems with subject matching, is well within the range of the potential biases in the study. The authors of the study had a reasonable basis for making their original hypothesis and many of the problems with the study are inherent in a study of this type. If they had found substantial, several-fold differences between the two groups and especially a substantial difference in the primary endpoint, then this might well have suggested this was an area worthy of investing further resources for investiga- tion using more robust and varied methodologies. Despite the study’s many serious weaknesses, the
- 51. 16 Changing priorities in nutrition authors and the press coverage emphasised the weak positive relationships, particularly the small appar- ent increase in relative risk associated with eating yoghurt or cottage cheese once a month. The results failed to support the primary hypothesis of higher galactose consumption in women prior to developing ovarian cancer. One could well imagine that a differ- ent set of authors might have presented the results of this same study in a different way. For example, authors with affiliation to the dairy industry might have concluded that it provides no evidence to sup- port the suggestion that high galactose intake causes ovarian cancer. Even if they reported the apparently positive data relating to yoghurt and cottage cheese they might have framed it much more conserva- tively, e.g. we cannot totally rule out the possibility that some dairy foods are very slightly increased in the case group, but this is highly likely to be a chance observation resulting from the crudeness of the methodology and the multiple testing. They might have noted the reduced activity of the transferase enzyme as a possible direct or indirect effect of the cancer or treatment. Given the very pronounced historical bias against the pub- lication of negative results, I wonder how the referees and the editorial board of The Lancet back in 1989 would have responded to this paper if it had been couched in these negative terms. Authors have gen- erally felt the need to emphasise positive findings in order to get their papers accepted in top journals. In the three decades since publication, Cramer’s hypothesis has spawned dozens of studies of differ- ent types: • More case-control studies. • Many cohort studies where dairy food and lactose are recorded in large groups of women and related to the subsequent development of ovarian cancer in a few of them. • Studies in which the effects of high galactose intake is studied in animals. • Laboratory studies looking at the effect of exposure of ovarian cells to high galactose concentrations. There have also been a number of attempts at aggregating the epidemiological studies (see meta- analysis in Chapter 5) to try and get a consensus of their findings. The most recently published of these meta-analyses that I have found was Liu et al. (2015). They used the results from no fewer than 19 cohort studies and found no statistically significant link between the intake of either lactose or individ- ual dairy foods like milk, cheese or yoghurt and the risk of ovarian cancer. Other meta-analyses have produced some just significantly positive results, although none of the large individual cohort studies that they amalgamate produces significant results. For example, Genkinger et al. (2006) reported the results obtained by pooling the results of 12 cohort studies involving a total of more than 550,000 women. They reported that women who ate 30 g/ day of lactose had marginally higher (19%) risk of ovarian cancer than those who consumed less than 10 g/day (500 ml of milk has about 20 g lactose). This difference was just statistically significant but well within the range of being due to potential bias. Five of the individual studies found that relative risk was increased in the lower lactose consumers but seven found that it was greater in the high lactose consumers, although in not one of the 12 individual studies was this difference statistically significant despite each involving tens of thousands of women. They found no associations with particular dairy foods like milk, cheese or yoghurt and ovarian can- cer. The consensus of evidence suggests that there is not likely to be a link between the consumption of yoghurt, other dairy foods or galactose and the risk of developing ovarian cancer. If there is any causal link then it is so tiny an influence that it is at or below the limits of detection by the methods currently available to nutritional scientists. Given this conclusion, there seems no realistic possibil- ity, either now or after many more similar studies, that any valid and unbiased recommendation could be made to women to alter their consumption of dairy foods in order to alter their risk of develop- ing ovarian cancer. Ovarian cancer is a relatively uncommon condition whose frequency increases with age and around 1 in 70 women will develop the condition during their lifetime. For example in one large Dutch study with older (postmenopausal) women about 40 women per 10,000 developed the condition over the 11.3 years of follow-up. Current epidemiological methods cannot definitively detect small increases in this risk (say 20%) and confi- dently attribute it to an association with a specific dietary factor.
- 52. 17 Key reference Despite the weakness of the evidence it contains, this paper by Cramer and his colleagues has helped to spawn hundreds of other papers over almost 3 decades without really advancing our understand- ing of the causes of ovarian cancer or our ability to make valid dietary recommendations to reduce it. Many more studies will probably be published in the future without any real prospect of changing that conclusion. KEY REFERENCE 1. Webb (14 July 2016) Webb, GP Health claims and scares I. Does eating yogurt really cause ovarian cancer? Dr Geoff Wordpress blog article https://drgeoffnutrition.wordpress. com/2016/07/14/health-claims-and-scares- i-does-eating-yogurt-really-cause-ovarian- cancer/
- 54. 19 2 Food selection INTRODUCTION AND AIMS OF THE CHAPTER Most of this book focuses upon food as a source of energy and nutrients, questions such as: • Which nutrients are essential and why? • How much of these nutrients do people need at various times of their lives? • How does changing the balance of nutrients eaten affect long-term health? This chapter is in a small way, an antidote to the necessary scientific reductionism of much of the rest of the book. The general aim of the chapter is to remind readers that “people eat food and not nutri- ents” and that nutrient content has only relatively recently become a significant factor in the making of food choices. Only in the latter part of the twen- tieth century did our knowledge of nutrient needs and the chemical composition of food become suffi- cient to allow them to be major influences upon food selection. A host of seasonal, geographical, social and eco- nomic factors determine the availability of different foods to any individual or group, whilst cultural and preference factors affect its acceptability. Some of these influences are listed in Table 2.1. If health promotion involves efforts to change people’s food choices, some understanding of the non-nutritional uses of food, and of the way non-nutritional factors interact to influence food choices, is essential. It is pointless devising an excellent diet plan or drawing up detailed dietary guidelines unless they are actually implemented. Diets or dietary recommendations that may seem ideal from a reductionist biological viewpoint may have little impact upon actual food choices. Some people may have very limited freedom to make food choices e.g. those living in institutions where all of Introduction and aims of the chapter 19 The biological model of food 20 Dietary and cultural prejudice 21 Food classification systems 22 Non-nutritional uses of food 27 The hierarchy of human needs 28 A model of food selection – “The hierarchy of availabilities model” 30 Physical availability 32 Economic availability 32 Cultural availability 37 “Gatekeeper” limitations on availability 43 A social–ecological model for food and activity decisions 45 Key references 46
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- 56. South Mountain Mountain Dundas John Morrow * South Quebec Lévis Lévis Mrs. Anne Wensley South Roxton Roxton Shefford A. Sanborn South Zorra Zorra, East Oxford, N. R. Thomas Cross * Sparta Yarmouth Elgin, S. R. John A. Eakins Speedie Sydenham Grey Wm. Speedie Speedside Eramosa Wellington, S. R. James Loughrin Spencer Cove Quebec Denis Maguire Spencerville Edwardsburgh Grenville, S. R. W. B. Imrie Spring Arbour Walsingham Norfolk J. W. Hazen Springbank E. Williams Middlesex, W. R. W. Wells Springfield Dorchester, South Elgin, E. R. W. H. Graves Springford Norwich Oxford, S. R. John Wood Springville North Monaghan Peterboro’ A. Goodfellow Staffa Hibbert Perth R. F. Rundle Stafford Stafford Renfrew Robert Childerhose Stamford Stamford Welland Ellen Wilson * † Stanbridge, East Stanbridge Missisquoi E. J. Briggs Standon Standon Dorchester John Nicholson * † Stanfold Stanfold Arthabaska James Huston Stanhope Barford Stanstead Alexander Murray Stanley’s Mills Chinguacousy Peel C. Burrell * † Stanstead Stanstead Stanstead B. F. Hubbard Starnesboro’ St. Antoine Abbé Chateauguay * Stayner Nottawasaga Simcoe, N. R. John McKeggie Stella Amherst Island Addington William Perceval Stevensville Bertie Welland Benjamin House * Stirling Rawdon Hastings, N. R. William Judd Stirton Peel Wellington, N. R. John Luxson Stittsville Goulburn Carleton J. S. Argue Stoco Hungerford Hastings, N. R. Francis Murphy Stonefield Chatham Argenteuil Owen Owens Stoneham Quebec B. Pattison * Stoney Creek Saltfleet Wentworth, S. R. Alva G. Jones Stoney Point Tilbury, West Essex H. Desjardins
- 57. Stornoway Winslow Compton Colin Noble † Stottville St. Johns William Burland * Stouffville Whitchurch York, N. R. Edwd. Wheler * Strabane Flamboro’, West Wentworth, N. R. Matthew Peebles * Straffordville Bayham Elgin, E. R. D. C. Swayne Strangford York York, E. R. Isaac Blain * Stratford South Easthope Perth L. T. O’Loane Strathallan East Zorra Oxford, N. R. John Lappin Strathburn Mosa Middlesex, W. R. Hugh McRae * Strathroy Caradoc Middlesex, W. R. * Streetsville Toronto Peel James E. Rutledge Stretton Reach Ontario, N. R. R. Stretton Stromness Sherbrooke Haldimand John Macdonald * † Stukeley Stukeley Shefford L. H. Brooks Sullivan Holland Grey William Buchanan Summerstown Charlottenburg Glengary David Summers Summerville Toronto Peel William Bemrose Sunbury Storrington Frontenac John McBride Sunnidale Sunnidale Simcoe, N. R. Alexander Gillespie Sutherland’s Corners Euphemia Lambton James Walker * † Sutton Sutton Brome G. C. Dyer Sweaburg West Oxford Oxford, S. R. James H. Hill * Sweetsburgh Dunham Missisquoi G. H. Sweet Switzerville Ernestown Addington Calvin W. Miller Sydenham Place Kingsey Drummond Joseph Millington * Sylvan Williams, West Middlesex, W. R. Robert Burns Tadousac Saguenay Joseph Radford Talbotville Royal Southwold Elgin, W. R. John Stacey * Tamworth Sheffield Addington W. R. Aylsworth Tannery West Montreal Hochelaga A. Desève Tapleytown Saltfleet Wentworth, S. R. J. Springstead Tara Arran Bruce John Tobey Tatlock Darling Lanark, S. R. James Guthrie, Sr. Tavistock South Easthope Perth George Matheson
- 58. Tecumseth Tecumseth Simcoe, S. R. A. N. Hipwell Teeswater Culross Bruce M. Hadwen Teeterville Windham Norfolk Thos. Edgeworth Telfer London Middlesex, E. R. Adam Telfer † Templeton Templeton Ottawa James Hagan Tempo Westminster Middlesex, E. R. A. Remey Tennyson Drummond Lanark, S. R. D. McGregor * † Terrebonne Terrebonne Terrebonne John McKenzie Tessierville Matane Rimouski J. E. Genereux Teston Vaughn York, W. R. George Wilson Teviotdale Minto Wellington, N. R. M. G. Miller Thamesford Nissouri, East Oxford, N. R. N. C. McCarty * Thamesville Camden Kent J. C. Collier Thanet Wollaston Hastings, N. R. B. McKillican Thistletown Etobicoke York, W. R. Richard Johnston Thomasburg Hungerford Hastings, N. R. W. W. Jones Thompsonville Tecumseth Simcoe, S. R. J. T. Schmietendorf Thornbury Collingwood Grey Isaac N. Hurd Thorndale Nissouri, West Middlesex, E. R. Thomas Harrison Thorne Thorne Pontiac Joseph Hill * Thornhill Vaughan York, W. R. Josiah Purkiss Thornton Innisfil Simcoe, S. R. John Henry * Thorold Thorold Welland Jacob Keefer Thorold Station Grantham Lincoln S. M. Stephens * Three Rivers Three Rivers T’n of Three Rivers C. K. Ogden Thurlow Thurlow Hastings, S. R. William T. Casey * † Thurso Lochaber Ottawa G. W. Cameron * Tilbury East Tilbury, East Kent James Smith Tiverton Bruce Bruce N. McInnes Toledo Kitley Leeds, N. R. Mrs. C. A. McLean Topping North Easthope Perth S. Crozier Torbolton Torbolton Carleton H. Younghusband Tormore Albion Peel William Graham * Toronto York City of Toronto Joseph Lesslie Totnes Ellice Perth G. H. Dennstedt Tottenham Tecumseth Simcoe, S. R. Townsend Centre Townsend Norfolk Hiram Slaght
- 59. Trafalgar Trafalgar Halton James Appelbe Treadwell Plantagenet Prescott Humphrey Hughes Trecastle Maryboro’ Perth D. Scroggie Tremblay Tremblay Chicoutimi Marcel Côté Trenholm Kingsey Drummond Simon Stevens * Trenton Murray Hastings, S. R. James Cumming † Trois Pistoles Trois Pistoles Témiscouata T. P. Pelletier Trois Saumons St. Jean Port Joli L’Islet G. C. Caron Trout River Godmanchester Huntingdon James Marshall Trowbridge Elma Perth G. Code Troy Beverley Wentworth, N. R. Trudell Tilbury, West Essex Henry Richardson Tuam Tecumseth Simcoe, S. R. P. H. Derham * Tullamore Toronto Gore Peel J. Mulligan Tuscarora Onondaga Brant, E. R. Tweed Hungerford Hastings, N. R. Richard Marshall Tweedside Saltfleet Wentworth, S. R. Gilbert Johnson Tyrconnell Dunwich Elgin, W. R. Peter Cameron Tyrone Darlington Durham, W. R. John T. Welch Udora Scott Ontario, N. R. S. Umphrey Uffington Draper Victoria A. Thompson Ulster Wawanosh Huron George McKay Ulverton Durham Drummond James Miller Umfraville Dungannon Hastings, N. R. D. Kavanagh Underwood Bruce Bruce J. H. Coulthard Union Yarmouth Elgin, E. R. S. U. Willson Unionville Markham York, E. R. George Eakin Upnor Carden Victoria Thomas Tressidder Utica Reach Ontario, N. R. Wm. McPherson Utterson Stephenson Victoria James F. Hanes * Uxbridge Uxbridge Ontario, N. R. George Wheler Vaillancourt Dionne L’Islet W. F. Vaillancourt Valcartier Valcartier Quebec Charles S. Wolff Valcourt S. Ely Shefford Jos. Roussin
- 60. Valetta Tilbury, East Kent J. Richardson † Valleyfield Beauharnois Beauharnois John Madden Vandecar Oxford, East Oxford, S. R. Thomas H. Arnell * Vankleek Hill Hawkesbury Prescott Duncan McDonell † Varennes Varennes Verchères J. N. A. Archambeault Varna Stanley Huron Josiah B. Secord † Vaudreuil Vaudreuil Vaudreuil F. Desalles Bastien Veighton Cumberland Russell John McVeigh Vellore Vaughan York, W. R. Henry Frank Venice Noyan Iberville James Lewis Vennachar Abinger Frontenac Charles McKenyon Ventnor Edwardsburgh Grenville, S. R. John Gamble Verchères Verchères Verchères Trefflé Lussier Verdun Huron Bruce J. Colling Vernon Osgoode Russel Vernonville Haldimand Northumberl’d, W. R. Henry Terry Verona Portland Frontenac Joseph Watson Versailles St. Grégoire Iberville Isidore Marcoux Vesta Brant and Elderslie Bruce Robert Cannon Vicars Havelock Huntingdon James Bustard Victoria Corners Reach Ontario, N. R. John Henderson Victoria Square Markham York, E. R. James A. Oves * Vienna Bayham Elgin, E. R. John P. Macdonald Viger Viger Témiscouata Thomas Tremblay Viger Mines Chester Arthabaska L. Labrèche Village des Aulnaies St. Roch des Aulnaies L’Islet A. Dupuis Village Richelieu St. Mathias Rouville G. Franchère Villanova Townsend Norfolk John McLaren Vincennes St. Luc Champlain P. Lacourcière Vine Innisfil Simcoe, S. R. A. Jameson Violet Ernestown Addington D. W. Perry Virgil Niagara Lincoln James M. Bristol * Vittoria Charlotteville Norfolk Simpson McCall * Vroomanton Brock Ontario, N. R. S. Parrish
- 61. Wakefield Wakefield Ottawa James McLaren * Walkerton Brant Bruce Malcolm McLean Wallace Wallace Perth D. M. Williams * Wallaceburg Chatham Kent Daniel Johnson * Wallacetown Dunwich Elgin, W. R. John McKillop Wallbridge Sidney Hastings, S. R. Stephen Miller Walsh Charlotteville Norfolk Mrs. M. A. Owen Walsingham Walsingham Norfolk Henry L. Kitchen Walter’s Falls Holland Grey John Walter Waltham Waltham Pontiac John Landon Walton Grey Huron George Bigger Wanstead Plympton Lambton John Dewar Warden Shefford Shefford E. D. Martin * Wardsville Mosa Middlesex, W. R. Henry R. Archer * Warkworth Percy Northumberl’d, E. R. Israel Humphries Warner Caistor Lincoln T. W. Smith Warrington Nottawasaga Simcoe, N. R. George Randolph Warsaw Dummer Peterboro’ Thomas Choat † Warwick, L. C. Warwick Arthabaska L. T. Dorais Warwick, U. C. Warwick Lambton James Menerey Washington Blenheim Oxford, N. R. Daniel Wakefield * Waterdown Flamboro’, East Wentworth, N. R. James B. Thompson * Waterford Townsend Norfolk G. W. Park * Waterloo, L. C. Shefford Shefford Jonathan Robinson * Waterloo, U. C. Waterloo, North Waterloo, N. R. C. Kumpf Waterloo, Kingston Kingston Frontenac Joseph Northmore Waterville Compton Compton Charles Brooks Watford Warwick Lambton James Merry Watson’s Corners Dalhousie Lanark, N. R. James Purdon Waverley Flos Simcoe, N. R. A. Kettle Way’s Mills Barnston Stanstead E. S. Southmayd Weedon Weedon Wolfe Siméon Fontaine Welcome Hope Durham, E. R. Wm. Strike * Welland Crowland Welland Thomas Burgar Welland Port Gainsboro’ Lincoln Samuel Holmes
- 62. * Wellesley Wellesley Waterloo, N. R. John Zoeger * Wellington Hillier Prince Edward Donald Campbell * Wellington Square Nelson Halton Robert Menzies Wellman’s Corners Rawdon Hastings, N. R. T. H. Clare West Arran Arran Bruce John Biggar West Brome Brome Brome S. L. Hungerford West Brook Kingston Frontenac Benjamin Clark West Broughton Broughton Beauce J. St. Hilaire Westbury Westbury Compton Allen Lothrop West Essa Essa Simcoe, S. R. Thomas Drury * † West Farnham Farnham Missisquoi L. G. Foisy Westfield Wawanosh Huron H. Help * West Flamboro’ Flamboro’ Wentworth, N. R. John Percy West Huntingdon Huntingdon Hastings, N. R. Philip Luke West Huntley Huntley Carleton Edward Horan West Lake Hallowell Prince Edward Henry Lambert West McGillivray McGillivray Huron William Fraser Westmeath Westmeath Renfrew D. B. Warren * Weston York York, W. R. Robert Johnston West Osgoode Osgoode Russell John C. Bower Westover Beverley Wentworth, N. R. B. McIntosh Westport North Crosby Leeds, S. R. Walter Whalen West Potton Potton Brome C. Gilman West’s Corners Mornington Perth John Pierson West Shefford Shefford Shefford John N. Mills West Winchester Winchester Dundas William Bow Westwood Asphodel Peterboro’ Revd. M. A. Farrar West Woolwich Woolwich Waterloo, N. R. Peter Winger Wexford Scarboro’ York, E. R. J. T. McBeath Wheatland Wickham Drummond Edward McCabe Wheatly Mersea Essex W. Buchanan * Whitby Whitby Ontario, S. R. David Smith Whitehurst Elizabethtown Town of Brockville John Bell White Lake McNab Renfrew John Paris White Rose Whitchurch York, N. R. Jared Lloyd Whitevale Pickering Ontario, S. R. Donald McPhee Whitfield Mulmur Simcoe, N. R. P. D. Henry
- 63. Whittington Amaranth Wellington, N. R. R. Bowsfield Wick Brock Ontario, N. R. James Brebner Wicklow Haldimand Northumberl’d, W. R. C. E. Ewing Widder Bosanquet Lambton Adam Duffus * Widder Station Bosanquet Lambton Thos. Kirkpatrick Wilkesport Sombra Lambton William Kimball Willetsholme Pittsburgh Frontenac Williams Williams, East Middlesex, W. R. Colin McKenzie Williamstown Charlottenburg Glengary Duncan McLennan Williscroft Elderslie Bruce George Williscroft Willowdale York York, W. R. Jacob Cumner Willowgrove Oneida Haldimand John Doyle Wilmur Loughboro’ Frontenac Marvin Holden * Wilton Ernestown Addington Sydney Warner Wimbledon Sandwich Essex John Jessop Winchelsea Usborne Huron A. Smith Winchester Winchester Dundas C. T. Casselman Winchester Springs Williamsburg Dundas Windham Centre Windham Norfolk James Robertson * Windsor Sandwich, East Essex Alex. H. Wagner Windsor Mills Windsor Richmond C. E. Wurtele Winfield Peel Wellington, N. R. James Young Wingham Turnberry Huron E. Foley Winterbourne Woolwich Waterloo, N. R. Elizabeth Gordon Wisbeach Warwick Lambton Joanna Bowes Woburn Scarboro’ York, E. R. John Irving Wolfe Island Wolfe Island Frontenac George Malone Wolfstown Wolfstown Wolfe J. Pelletier Wolverton Blenheim Oxford, N. R. James Currey * Woodbridge Vaughan York, W. R. John F. Howell Woodburn Binbrook Wentworth, S. R. William Ptolemy Woodford Sydenham Grey John Hill Woodham Blanshard Perth Walker Unwin Woodlands Oznabruck Stormont R. H. Stewart † Woodside Halifax Megantic Thomas Wood Woodslee Maidstone Essex W. S. Lindsay * Woodstock Blandford Oxford, N. R. Chas. DeBlaquière
- 64. Woodville Eldon Victoria John Morrison Wooler Murray Northumberl’d, E. R. Reuben Scott † Wotton Wotton Wolfe C. Ducharme Wright Wright Ottawa Joshua Ellard * Wroxeter Howick Huron Cyrus Carroll Wyandott Maryboro’ Wellington, N. R. G. Thomlinson Wyebridge Tiny Simcoe, N. R. James Plewes * Wynford Nichol Wellington, N. R. John R. Wissler * Wyoming Plympton Lambton John Anderson * † Yamachiche Machiche St. Maurice Elie Lacerte * † Yamaska Yamaska Yamaska E. G. Dugré * Yarker Camden Addington J. A. Shibley Yarmouth Centre Yarmouth Elgin, E. R. William Mann * York Seneca Haldimand Charles L. Hudson York Mills York York, E. R. John Hogg York River Faraday Hastings, N. R. James Cleak * Yorkville York York, E. R. James Dobson Young’s Point Smith Peterboro’ John Young Zephyr Scott Ontario, N. R. George W. Hunter Zetland Turnberry Huron L. J. Brace Zimmerman Nelson Halton Robert Miller Zurich Hay Huron Louis Vauthier
- 65. [1] Late Ashfield. [2] Late Caistor. [3] Late Lippincott. [4] Closed during winter. [5] Late Bentinck. [6] Open during summer only. [7] Late Artemesia. [8] Late Cavagnol. [9] Late Proton. [10] Late Irish Creek. [11] Late Glenelg. [12] Formerly Merton. [13] Late St. Vincent. [14] Late Newland. [15] Formerly Tring.
- 66. List of Post Offices Closed between 1st January, 1865, and 1st January, 1866, inclusive. NAME OF POST OFFICE. COUNTY. REMARKS. Allan Park Grey Amulree Perth Bois de L’Ail Lotbinière Carlton, West York Clareview Addington Edgeworth Kent Elphin Lanark Ennis Lambton Farmington Wellington Fish Creek Perth Foxboro’ Hastings Fulton Lincoln Homer Lincoln Kintail Huron L’Acadie Station St. Johns Morrisdale Huron Peterson Victoria Rouge Hill Ontario Ryckman’s Corners Wentworth St. François de Sales Laval Established 1st April, 1865, and closed 1st January, 1866. Strathglass Stormont
- 67. List of Changes in the Names of Post Offices, between 1st January, 1865, and 1st January, 1866, inclusive. LATE NAME OF OFFICE. COUNTY. NEW NAME SELECTED. Caistor Lincoln Attercliffe Cavagnol Vaudreuil Hudson East Frampton Dorchester Hemison Isle du Pads Berthier Isle Dupas Proton Grey Inistioge St. Vincent Grey Meaford Tring Beauce St. Victor de Tring Bentinck Grey Durham Lippincott York Brockton Ashfield Huron Amberley Newland York Mount Albert South Potton Brome Mansonville-Potton
- 68. LIST OF POST OFFICES IN CANADA, ON 1st JANUARY 1866, ARRANGED ACCORDING TO ELECTORAL COUNTIES. Addington County. Baldwin. Bath. Camden East. Cawdor. Centreville. Colebrook. Croydon. Denbigh. Desmond. Emerald. Enterprise. Erinsville. Flinton. Glastonbury. Kaladar. Millhaven. Morven. Moscow. Newburgh. Odessa. Overton. Stella. Switzerville. Tamworth. Violet. Wilton. Yarker. Argenteuil County. Avoca. Bethune. Britonville. Brownsburg. Carillon. Cushing. Dalesville. Dunany. Geneva. Grenville.
- 69. Harrington East. Lachute. Lakefield. Mille Isles. Muddy Branch. Pointe aux Chênes. Rockland. St. Andrews East. Shrewsbury. Stonefield. Arthabaska County. Arthabaska Station. Blandford. Bulstrode. Chester. Domaine de Gentilly. East Arthabaska. East Chester. Maddington. St. Christophe d’Arthab’ka. St. Clothilde. St. Patrick’s Hill. Stanfold. Viger Mines. Warwick, East. Bagot County. Actonvale. St. Dominique. St. Ephrem d’Upton. St. Hélène de Bagot. St. Hugues. St. Liboire. St. Pie. Ste. Rosalie. St. Simon de Yamaska. St. Théodore. Beauce County. Broughton. Jersey, River Chaudière. Kenebec Line. La Beauce. Lambton. Marlow. River Gilbert. St. Ephrem de Tring. St. Evariste de Forsyth.
- 70. St. François. St. Frédéric. St. George. St. Joseph. St. Victor de Tring. West Broughton. Beauharnois County. Beauharnois. Melocheville. St. Etienne de Beauharnois St. Louis de Gonzague. St. Stanislas de Kostka. St. Timothée. Valleyfield. Bellechasse County. Armagh. Beaumont. Buckland. St. Charles, River Boyer. St. Gervais. St. Lazare. St. Michel. St. Raphael. St. Vallier. Berthier County. Berthier (en haut). Isle Dupas. Lanoraie. Lavaltrie. St. Barthélemi. St. Cuthbert. St. Gabriel de Brandon. St. Norbert. Bonaventure County. Bonaventure (Sub.) Carleton. Cross Point. Maria. Matapédiac. New Carlisle. New Richmond. Paspébaic. Port Daniel. Runneymede.
- 71. Shigawake. Shoolbred. Brant, East Riding. Cainsville. Glen Morris. Harrisburg. Paris. Paris Station. Rosebank. St. George. Tuscarora. Brant, West Riding. Brantford. Burford. Burtch. Cathcart. Falkland. Harley. Kelvin. Mohawk. Mount Vernon. New Durham. Newport. Oakland. Onondaga. Scotland. Brockville, Town. Addison. Brockville. Greenbush. Lyn. Whitehurst. Brome County. Abercorn. Adamsville. Bolton Forest. Brigham. Brome. Bromemere. East Bolton. East Farnham. East Potton. Farnham Centre. Fulford.
- 72. Glensutton. Iron Hill. Knowlton. Mansonville-Potton. Nashwood. North Sutton. Owl’s Head. South Bolton. Sutton. West Brome. West Bolton. Bruce County. Arkwright. Bervie. Burgoyne. Carlsruhe. Carnegie. Chepstow. Colpoy’s Bay. Dumblane. Dunkeld. Ellengowan. Elmwood. Elsinore. Formosa. Glammis. Glenlyon. Greenock. Gresham. Hepworth. Inverhuron. Invermay. Kincardine. Kinloss. Kinlough. Langside. Lisburn. Lovat. Lucknow. Lurgan. Malta. Normanton. North Bruce. Outram. Paisley. Pine River. Pinkerton. Reekie. Ripley. Riversdale. Saugeen.
- 73. Scone. Tara. Teeswater. Tiverton. Underwood. Verdun. Vesta. Walkerton. West Arran. Williscroft. Carleton County. Antrim. Ashton. Bell’s Corners. Carp. Diamond. Fitzroy Harbor. Hazledean. Hubbell’s Falls. Huntley. Kars. Kinburn. Long Island Locks. Malakoff. Manotick. Marathon. March. Merivale. Munster. North Gower. Panmure. Richmond, West. South Gloucester. South March. Stittsville. Torbolton. West Huntley. Chambly County. Boucherville. Chambly Basin. Chambly Canton. Longueuil. St. Bruno. St. Hubert. St. Lambert, Montreal. Champlain County.
- 74. Batiscan. Batiscan Bridge. Cap Magdeleine. Champlain. Ste. Anne de la Pérade. St. Maurice. St. Narcisse. St. Prosper. St. Stanislas. St. Tite. Vincennes. Charlevoix County. Isle aux Coudres (Sub.) La Petite Rivière St. François (Sub.) Les Eboulemens. Murray Bay. Port au Persil. St. Agnès. St. Fidèle. St. Irénée. St. Paul’s Bay. Settrington. Chateauguay County. Allan’s Corners. Chateauguay. Chateauguay Basin. Howick. North Georgetown. Norton Creek. Ormstown. Russeltown. St. Jean Chrysostôme. Ste. Martine. Ste. Philomène. St. Urbain. Starnesboro’. Chicoutimi County. Bagotville. Chicoutimi. Grande Baie. Labarre. L’Anse au Foin. L’Anse St. Jean. Laterrière. Roberval. Tremblay.
- 75. Compton County. Birchton. Brookbury. Bulwer. Compton. Cookshire. East Clifton. East Hereford. Eaton. Gould. Hereford. Johnville. Lake Megantic. Maple Leaf. Martinville. Moe’s River. Robinson. St. Malo. St. Romaine. St. Venant. Sawyerville. Stornoway. Waterville. Westbury. Cornwall Town. Cornwall. Mille Roches. St. Andrews, West. Dorchester County. Cranbourne. Frampton. Hemison. St. Anselme. St. Bernard. Ste. Claire. Ste. Hénédine. St. Isidore. St. Malachie. Ste. Marguerite. Standon. Drummond County. Drummondville, East. French Village. Headville. Kingsey.
- 76. Kingsey Falls. L’Avenir. Leonard’s Hill. Ruisseau des Chênes. St. Guillaume d’Upton. South Durham. Sydenham Place. Trenholm. Ulverton. Wheatland. Dundas County. Dixon’s Corners. Dunbar. East Williamsburgh. Inkerman. Iroquois. Morewood. Morrisburgh. North Mountain. North Williamsburgh. Ormond. South Mountain. West Winchester. Winchester. Winchester Springs. Durham, East Riding. Baillieboro’. Ballyduff. Bethany. Brunswick. Burton. Canton. Cavan. Elizabethville. Franklin. Janetville. Lifford. Millbrook. Mount Pleasant. Perrytown. Port Hope. Welcome. Durham, West Riding. Bowmanville. Cæsarea. Cartwright.
- 77. Clarke. Enniskillen. Hampton. Haydon. Kendal. Kirby. Leskard. Newcastle. Orono. Port Granby. Port Hoover. Tyrone. Elgin, East Riding. Aylmer, West. Bayham. Belmont. Dexter. Eden. Grovesend. Luton. Lyons. Mapleton. New Sarum. Orwell. Port Bruce. Port Burwell. Port Stanley. St. Thomas, West. Salem. Sparta. Springfield. Straffordville. Union. Vienna. Yarmouth Centre. Elgin, West Riding. Aldboro’. Clachan. Cowal. Crinan. Eagle. Fingal. Frome. Iona. Largie. Port Talbot. Rodney. Talbotville Royal. Tyrconnell.
- 78. Wallacetown. Essex County. Amherstburgh. Blytheswood. Colchester. Comber. Gosfield. Harrow. Kingsville. Leamington. Maidstone. Mersea. North Ridge. Olinda. Rochester. Ruthven. Sandwich. Stoney Point. Trudell. Wheatly. Wimbledon. Windsor. Woolslee. Frontenac County. Arden. Ardoch. Battersea. Bellrock. Birmingham. Brewer’s Mills. Cloyne. Collin’s Bay. Deniston. Elginburgh. Fermoy. Gemley. Glenburne. Glenvale. Hardinge. Harrowsmith. Howe Island. Inverary. Kingston Mills. Loughboro’. Mountain Grove. Murvale. Ompah. Parham. Petworth.
- 79. Pittsferry. Portsmouth. Railton. Sharpton. Sunbury. Vennachar. Verona. Waterloo, Kingston. Westbrooke. Willetsholme. Wilmur. Wolfe Island. Gaspé County. Barachois de Malbay. Cap Chat (Sub.) Cape Cove. Douglastown. Fox River. Gaspé Basin. Grande Grève. Grand River. Magdalen Islands. Peninsula, Gaspé. Percé. Point St. Peter. Ste. Anne des Monts. Sandy Beach. Glengary County. Alexandria Athel. Breadalbane. Dalhousie Mills. Denvegan. Glennevis. Kirkhill. Laggan. Lancaster. Loch Garry. Lochiel. Martintown. North Lancaster. Notfield. Rivière Raisin. St. Raphael, West. Saudfield. Skye. Summerstown. Williamstown.
- 80. Grenville, North Riding. Bishop’s Mills. Burritt’s Rapids. Easton’s Corners. Heckstone. Jasper. Kemptville. Kilmarnock. Merrickville. Oxford Mills. South Gower. Grenville, South Riding. Algonquin. Centre Augusta. Charleville. Edwardsburgh. Maitland. Prescott. North Augusta. Shanly. Spencerville. Ventnor. Grey County. Allan Park. Alvanley. Ayton. Berkeley. Blantyre. Cape Rich. Chatsworth. Cedarville. Clarksburg. Cornabuss. Craigleith. Crawford. Daywood. Dromore. Dundalk. Durham. Egremont. Epping. Eugenia. Feversham. Flesherton. Glascott. Griersville. Hanover.
- 81. Heathcote. Hoath-head. Holstein. Horning’s Mills. Inistioge. Johnson. Kilsyth. Latona. Leavens. Leith. McIntyre. Marmion. Massie. Maxwell. Meaford. Melancthon. Mount Forest. Neustadt. North Keppel. Orchard. Osprey. Owen Sound. Oxenden. Pomona. Priceville. Ravenna. Ronaldsay. Sarawak. Shelburne. Shrigley. Singhampton. Speedie. Sullivan. Thornbury. Walter’s Falls. Woodford. Haldimand County. Balmoral. Black Heath. Byng. Canboro’. Canfield. Cayuga. Cheapside. Decewsville. Dufferin. Dunnville. Erie. Fisherville. Gifford. Hagersville.
- 82. Hullsville. Indiana. Jarvis. Lowbanks. Mount Healy. Nanticoke. North Seneca. Oneida. Port Maitland. Rainham. Rainham, Centre. Selkirk. Seneca. South Cayuga. Stromness. Willow Grove. York. Halton County. Acton. Appleby. Ashgrove. Boyne. Bronte. Campbellville. Cumminsville. Drumquin. Esquesing. Georgetown. Glen William. Hornby. Kilbride. Limehouse. Lothian. Lowville. Milton, West. Nassagiweya. Nelson. Norval. Oakville. Omagh. Palermo. Port Nelson. Scotch Block. Silver Creek. Trafalgar. Wellington Square. Zimmerman. Hamilton (City.) Hamilton.
- 83. Hastings, North Riding. Bannockburn. Bark Lake. Bogart. Bridgewater. Cooper. Glanmire. Harold. Ivanhoe. Lime Lake. Madoc. Malone. Marlbank. Marmora. Maynooth. Mill Bridge. Moira. Moneymore. Purdy. Queensborough. Shanick. Stirling. Stoco. Thanet. Thomasburg. Tweed. Umfraville. Wellman’s Corners. West Huntingdon. York River. Hastings, South Riding. Belleville. Blessington. Cannifton. Frankford. Halloway. Lonsdale. Marysville. Melrose. Mill Point. Plainfield. Roslin. Shannonville. Thurlow. Trenton. Wallbridge. Hochelaga County.
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