Appetiser:

Big Babies Become Obese Adults

Starting off as a big baby may not be so good for you when you grow up: a new study (1) has found that the largest babies, or those who grow fastest are more likely to become overweight adults. The British Medical Journal carried out a review of the association between infant growth during the first two years of life and obesity in adulthood, and all studies were found to be consistent. Prevention of obesity may therefore need to start very early.



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Main Course:

Diet and Alzheimer's Disease

Another recent dietary study (2) links a 'high fat' diet with the amyloid-beta (Abeta) deposits that cause Alzheimer's disease (AD) in the brains of mice. Previous studies have linked the consumption of cholesterol and saturated fats with Abeta deposition. The difference with this new study is the low carbohydrate content of the diet that the mice were given.



The principle that dietary fat might play a relatively passive role in metabolism and that the distribution of fat is regulated by the hormonal state stimulated by carbohydrate is standard basic biochemistry knowledge, but remains an under-appreciated factor in many studies, possibly due to the emphasis on low-fat recommendations of nutritional agencies. Because of the requirement of brain cells for glucose (or ketones) for energy metabolism and, in particular, because of the involvement of insulin in regulating a proteolytic enzyme in Abeta production, it is relevant to inquire about the role of macronutrient composition in the diet in AD. In doing so, the medical research world seems to be gradually getting closer to the fact that many people eating according to their blood group have known for a long time: sometimes dietary carbohydrate restriction can be part of a collection of factors that reduce inflammation. What doesn't seem to be appreciated in most diet studies is how other research shows that individuals of blood groups A and B are more prone to Alzheimer's disease than O and AB due to a different reason: a higher stress response to cortisol (3).



The authors of the study conclude: "a diet rich in saturated fats and low in carbohydrates can actually reduce levels of Abeta. Therefore, dietary strategies aimed at reducing Abeta levels should take into account interactions of dietary components and the metabolic outcomes, in particular, levels of carbohydrates, total calories, and presence of ketone bodies should be considered." The description 'high fat diet' is thus an inadequate way to characterize a diet: one must also specify the level of carbohydrate.



Looking for a reason for this, the article postulates: "evidence suggests that the primary genetic risk factor for late onset AD, the epsilon4 allele of apolipoprotein E, may have been selected against in populations with long historical exposure to agriculture." Individuals with this genotype are more prone to AD. The gene that did better with exposure to agriculture was the blood group A gene, which expressed in people who survived on a lower fat diet. Reduced levels of intestinal alkaline phosphatase in individuals of blood group A and AB means that they cannot digest fat well in their diet, but they may be able to better tolerate complex carbohydrate. Conversely individuals of blood group O and B may be able to tolerate more dietary fat, and less carbohydrate - the diet which gave less Abeta deposition in the study (on mice).



The study also says: "foods rich in carbohydrates are relatively recent additions to the human diet and are likely to be more evolutionarily discordant than high fat diets. Therefore, the recent evolutionary switch to high carbohydrate diets may play an important role in development of AD". In terms of blood groups, this is more likely to be true with individuals of blood groups O and B, but those with blood groups A and AB may not benefit from the high fat levels seen in this study.



Perhaps we should get away from the principle that “you are what you eat,” and replace it with the idea that “you are what you do with what you eat.”





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Dessert:

Reduce That Sweet Tooth With Weight Loss

Losing weight sensibly can reduce sugar cravings: In a recently published study (4) ten women were tested to see how quickly they found repeated eating or drinking of a sweet substance to be unpalatable after fasting overnight. They were then put on a weight loss diet (composed of 50% carbohydrate, 25% protein and 25% fat). After 3 months they had all lost weight, most had reduced their BMI by over 5%, but also all felt satiated earlier and withdrew from ingesting the sweet substance more quickly than before they started dieting.



The authors conclude: "Maintaining a lowered set-point, by consuming a sensible diet that promotes satiety and gradual weight loss, may be the key for long-term success, as the body strives to maintain a body weight close to that set-point by reducing food intake and enhancing energy expenditure."



This study shows that a standard calorie-controlled weight loss programme will eventually reduce the amount of sweets that the dieter craves before feeling satiated.



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References:



(1) Baird J, Fisher D, Lucas P, et. al:

Being big or growing fast: systematic review of size and growth in infancy and later obesity

BMJ 2005 331: 929



(2) Van der Auwera I, Wera S, Van Leuven F, Henderson ST:

A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer's disease

2005 Nutr Metab (Lond) 2005. 2:28



(3) Complete Blood Type Encyclopedia



(4) Frankham P, Gosselin C, Cabanac M:

Diet induced weight loss accelerates onset of negative alliesthesia in obese women

BMC Public Health 2005, 5:112