Fatty liver disease used to be associated with alcoholism but it is no longer restricted to heavy drinkers. Our calorie-rich but nutrient-poor diet has led to an epidemic of nonalcoholic fatty liver disease (NAFLD) that tracks our rising obesity and diabetes rates (1). Autopsies and ultrasound studies have shown that up to 75% of the obese and 70-85% of type 2 diabetics have fatty livers. And the low-profile but essential nutrient choline appears to provide the solution to the problem (1, 2).

What is NAFLD?

NAFLD develops in two stages (1). In the first stage fat accumulates in the liver. This fat can come from several sources — free fatty acids released into the blood by fat tissue, lipogenesis in the liver from carbohydrates (especially fructose from HFCS or table sugar), and dietary fats carried to the liver by chylomicron remnants. Fatty liver disease is a silent epidemic because its first stage, fat accumulation, generally doesn′t produce overt symptoms.

Unfortunately, the accumulated fat can be damaged by reactive oxygen species, especially if there is a lack of fat-soluble antioxidants and an excess of polyunsaturated fatty acids vulnerable to lipid peroxidation. Oxidative stress leads to the second stage, an inflammatory response that is made worse by our dietary omega-6 / omega-3 imbalance (3). The end result of the second stage is scarring and potential liver failure or cancer.

The role of choline in NAFLD

A healthy liver prevents the accumulation of fat and its associated complications by packaging excess triglycerides in very low density lipoproteins (VLDLs) and releasing them into the blood stream. Making VLDL particles requires phosphatidylcholine (lecithin), a choline-containing phospholipid. A shortage of choline prevents the liver from making VLDLs and delivering its fat stores to the appropriate tissues.

Phosphatidycholine can be made from the precursor phosphatidylethanolamine; choline is simply ethanolamine with three methyl groups at the nitrogen atom. But ethanolamine has to come from the diet as well, and its conversion to choline additionally requires the amino acid methionine, a methyl group donor. For this reason increasing methionine consumption also improves fatty liver disease.

Liver, eggs and wheat germ would be the best dietary sources of choline. But liver does not play a significant role in the North American diet, and egg consumption has decreased because of our cholesterol phobia. Not surprisingly then, nutrition surveys show that most Americans consume far less choline than the recommended Adequate Intakes, 425 mg/day for women and 550 mg/day for men (2).

Choline doesn′t just help prevent NAFLD; it is also needed for neurotransmitter synthesis, cell membrane signalling and methyl group metabolism (2). Choline deficiency is therefore a major health hazard. We need to increase consumption of this important nutrient but, judging by the obesity and diabetes trends, society isn′t getting any closer to a healthy diet. Supplementation with lecithin is an effective and affordable way to get enough choline.

Sources

1. Masterjohn C. Nonalcoholic fatty liver disease — a silent epidemic of nutritional imbalance. Weston A Price Foundation. Apr. 1, 2011.
   http://www.westonaprice.org/health-issues/nonalcoholic-fatty-liver-disease/pdf
2. Zeisel SH, da Costa K.-A. Choline: An essential nutrient for public health. Nutr Rev 2009;67(11):615-623.
   http://www.fasebj.org/content/5/7/2093.full.pdf
3. Beierbeck H. Increase omega-3 polyunsaturated fatty acids and prevent cardiovascular disease.
   http://www.naturalnews.com/028131_omega-3s_cardiovascular_disease.html

The last few decades have seen a dramatic rise in obesity rates and type 2 diabetes cases. There is in fact a causal connection between the two, and that link is chronic low-grade inflammation (1-4). Inflammation leads to insulin resistance — an inadequate response of tissues like liver, fat cells and skeletal muscle to insulin. The pancreas responds by increasing insulin secretion but, once it can no longer compensate for the decreased sensitivity, the result is full-blown type 2 diabetes.

The role of insulin

Insulin enables glucose uptake by skeletal muscle and fat cells. The hydrophilic glucose gets taken across the hydrophobic plasma membrane by glucose transporters called GLUT4. These GLUT4s are part of lipid vesicles (containers) inside the cell. Insulin binding to its receptor leads to the fusion of these GLUT4 vesicles with the plasma membrane, exposing their transporters for glucose uptake.

Even though liver cells have insulin-independent glucose transporters (GLUT2s), insulin also regulates liver glucose levels — it inhibits glycogenolysis (breakdown of glycogen to glucose) and gluconeogenesis (synthesis of glucose from non-carbohydrate sources), preventing glucose release from liver stores when plasma glucose levels are high.

Insulin also affects the release of free fatty acids from fat cells by inhibiting the breakdown (lipolysis) of triglycerides (TGs) to fatty acids and glycerol, preventing fatty acid release from fat stores while plasma glucose levels are high.

Because of insulin′s central role in regulating glucose and fatty acid supply insulin resistance has serious health consequences, one of which is type 2 diabetes.

The role of inflammation in insulin resistance

Fatty acids taken up by cells are either stored as triglycerides or used for fuel. When fatty acid influx exceeds the cell′s capacity to store or burn them, the result is cellular stress. Stressed cells secrete messenger molecules (chemokines) that recruit macrophages — immune system cells that dispose of dead and dying cells. These macrophages in turn secrete pro-inflammatory markers (cytokines) like TNF-α, initiating inflammation. Over months and years inflammation becomes chronic in the overweight and obese.

How does inflammation lead to insulin resistance? Insulin binding to cell receptors doesn′t automatically enable signaling and GLUT4 exposure. The cell has to phosphorylate certain tyrosine residues on the insulin receptor to enable signal transmission. Cells can also block signal transmission, for instance in response to nutrient excess, by phosphorylating serine instead of tyrosine residues.

It turns out that the enzymes catalyzing serine phosphorylation (and blocking insulin signaling) are also integral components of inflammatory pathways, i.e. inflammatory cytokines can activate these enzymes. The result is insulin resistance, not just in the stressed cells that attracted the macrophages but in all cells in tissues flooded with inflammatory cytokines.


This is obviously a very simplified description of a highly complex situation. In fact, the authors I quote point out that not every aspect of this process is fully understood. There is no question, however, that the development of insulin resistance in obesity is a two-step process. In the first step cells stressed by nutrient excess recruit macrophages, which in turn release inflammatory cytokines. In the second step these cytokines stimulate inflammatory pathways inside tissue cells that block insulin signal transmission.

Here is some of the supporting evidence:

• The obese have a greater rate of fatty acid flux (fatty acid storage and release) than lean individuals, increasing the likelihood of cellular stress
• Insulin-resistant cells contain greater numbers of fatty acid intermediates, indicating that the cells have trouble dealing with the increased fatty acid load
• Lean individuals can be made insulin-resistant by fatty acid infusion; stopping the infusion restores insulin sensitivity, demonstrating the importance of fatty acid flux
• Insulin resistance can also be prevented pharmacologically by suppressing the lipolysis of triglycerides to free fatty acids
• The obese show much higher levels of macrophages in fat tissues and much higher plasma levels of pro-inflammatory markers than the lean, confirming the connection between obesity and inflammation
• Anti-inflammatory drugs improve insulin sensitivity, showing that inflammation must be involved in the development of insulin resistance
• Genetically modified mice deficient in macrophage-derived TNF-α are protected against obesity-associated insulin resistance, demonstrating that the inflammation leading to insulin resistance originates in macrophages

Of course, obesity is by no means the only risk factor for type 2 diabetes. However, given its prevalence, obesity has to be a major cause. The good news is that insulin resistance can be reversed rather quickly by reducing one′s caloric intake; a negative energy balance improves insulin sensitivity even before weight loss is observed.

Sources

1. Schenk S, Saberi M, Olefsky JM. Insulin sensitivity: modulation by nutrients and inflammation. I Clin Invest 2008;118(9):2992-3002.
   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2522344/pdf/JCI0834260.pdf
2. Lumeng CN, Saltiel AR. Inflammatory links between obesity and metabolic disease. J Clin Invest 2011;121(6):2111-2117.
   http://dx.doi.org/10.1172/JCI57132
3. Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest 2006;116(7):1793-1801.
   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1483173/pdf/JCI0629069.pdf
4. Zeyda M, Stulnig TM. Obesity, inflammation, and insulin resistance — a mini-review. Gerontology 2009;55:379-386.
   http://dx.doi.org/10.1159/000212758

The July 2011 issue of Scientific American ran a rather interesting article on comparing the effectiveness of medical therapies (1). The piece, The Best medicine, is subtitled A quiet revolution in comparative effectiveness research just might save us from soaring medical costs. I doubt the savings in medical costs — every dollar spent on medical services is a dollar earned by someone providing those 'services', and those providers aren′t going to give up their slice of the pie without a fight. But I like the 'quiet revolution' in comparative effectiveness research (CER).

What′s so revolutionary about it? It doesn′t rely on randomized controlled trials (RCTs), the 'gold standard' that medical therapy is supposedly based on. Instead, investigators take advantage of the availablilty of detailed electronic medical records from millions of patients. Analyzing these data, researchers believe, yields results that are every bit as rigorous, at a fraction of the cost of RCTs.

RCTs are undoubtedly the best tool for the initial assessment of the safety and efficacy of new drugs. Randomly assigning study participants to either a treatment or a control group minimizes confounding differences; patients assigned by chance to either the treatment or the control groups are likely similar in all aspects except the therapy in question. Hiding these assignments from both patients and doctors (blinding) should minimize the placebo effect on the patient and bias on the part of the physician interpreting the 'treatment' results.

But once drugs are approved and prescribed, blinding and randomization become irrelevant. Therapies need to be assessed in real-world clinical settings where both doctors and patients know the treatment protocol. And detailed medical records contain all the relevant health, socioeconomic and other details for comparing patients known to be similar in every respect except the therapy in question.

The limitations of RCTs are well known (2), but they remain the 'gold standard' in medical research, the evidence to be given the greatest weight. Yet, much as Big Pharma would have us believe otherwise, most therapies aren′t supported by RCTs. The majority of drugs are prescribed for off-label use, and the majority of patients are taking drug combinations. Neither off-label use nor most drug combos are supported by RCTs. To quote one investigator, "There is a chasm between what gets done in practice and what science has shown" (1)

The insistence on RCT-based evidence as the ultimate authority is hypocritical and self-serving. It will undoubtedly be used to dismiss CER-based reassessments of existing therapies if those therapies are found to be ineffective. Insisting on RCT-backed evidence is also useful for discrediting 'alternative' therapies as 'unscientific'. Yet, RCTs are simply inappropriate in most areas of health and nutrition research. For example, it makes no sense to study supplementation with single nutrients in isolation; all nutrients are needed in the right amounts for optimal health.

Obviously we need, and should insist on, evidence-based therapies. But it is ridiculous to equate sound scientific evidence exclusively with randomized controlled trials. Let′s hope that this 'quiet revolution in comparative effectiveness research' takes a firm hold and relegates RCTs to the drug approval stage where they truly are the best strategy.

This new type of comparative effectiveness research may or may not alter medical practice and lower medical costs. But at least it should tell us, the patients, which of the available therapies are actually effective. If we are to be partners in making decisions that affect our health and wellbeing we need reliable information untainted by the financial interests of the medical/pharmaceutical establishment. By insisting on therapies that′ll actually do us some good we, the patients, might just help bring down medical costs.

Sources

1. Sharon Begley, The best medicine. A quiet revolution in comparative effectiveness research just might save us from soaring medical costs. Scientific American July 2011, 50-55.
2. Black N, Why we need observational studies to evaluate the effectiveness of health care. Br Med J 1996;312:1215.
   http://www.bmj.com/content/312/7040/1215.full

As you know, we have a system of hormones that adjust our energy intakes — through hunger and satiety signals — to match our energy needs. What happens if we override this control system and overeat? Could it be that our bodies simply increase their energy expenditure to dispose of any excess calories? A couple of recent articles (1,2) make me think that this may indeed be the case.

The first study (1) examined the effects of changes in portion sizes, numbers of daily eating/drinking occasions, and food energy densities on weight gains in adult Americans between 1977-1978 and 2003-2006. The investigators found that daily energy intake increased by an astonishing 570 Kcal during that period. Americans ate more often and they ate larger portions; the energy density of their food, on the other hand, didn′t change much.

The second study (2) estimated the independent contributions of diet, exercise and other lifestyle factors to weight change. More than 120,000 healthy non-obese Americans were followed between 1986 and 2006, and changes in lifestyle and weight were assessed every four years. The investigators found average weight gains of 0.8 lb per year; the top 5% increased their weight by about 3 lb annually. Physical activity in the least and most active 20% surveyed shaved ½ lb and 2½ lb, respectively, off the overall weight gain.

Back to that increase in energy intake of 570 Kcal per day (1). It is actually about twice as high as the 1971 to 2004 increases reported by the American Heart Association (3). According to those estimates, women increased their average daily energy consumption by 344 Kcal (from 1542 to 1886) and men by 243 Kcal (from 2450 to 2693). Even those increases are still substantial. If we assume that Americans ate enough food in the seventies to meet all their daily energy needs then these 243 (or 344 or 570) Kcal have to be considered excess energy. What does the body do with this excess?

Could these extra calories simply be stored as fat? That′s highly unlikely. Suppose that every day you stored 10 Kcal as fat. In one year you would put away an extra 3,650 Kcal, about the energy content of one pound of fat (3,500 Kcal). In other words, for every 10 Kcal stored per day you gain 1 lb per year. If your energy intake increased by 243 Kcal per day (the lowest of the three estimates) you would gain about 25 lb per year; this is about an order of magnitude more than the top weight gain of 3 lb quoted in ref. 2.

An increase in physical activity doesn′t use up this excess energy either. Even the top 20% — the most active — of the participants in the second study only managed to burn about 2½ lb per year (2), or about 25 Kcal per day. Again, this is only about one tenth of the lowest estimated consumption increase.

Since neither fat storage nor increased physical activity — nor for that matter a combination of the two — accounts for that energy excess, what happens to those extra calories? I can only see two other possibilities. Either they simply 'pass through', i.e. the extra food is not digested and absorbed, or the body increases its energy expenditure to use up that excess.

Could energy expenditure really rise in response to increased energy availability? I′ve never come across any discussion on that topic, and the authors of the papers I quoted don′t talk about it either. But if this is correct then it isn′t surprising that diets don′t work — the energy requirements you try to match or beat are a moving target.

Sources:

1. Duffey KJ, Popkin BM, Energy density, portion size, and eating occasions: Contributions to increased energy intake in the United States, 1977-2006.PLoS Medicine 2011;8(6):e1001050.
   http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.1001050
2. Mozaffarian D, Hao T, Rimm EB et al. Changes in diet and lifestyle and long-term weight gain in women and men. N Engl J Med 2011;364:2392-2404.
   http://anpron.eu/wp-content/uploads/2011/06/Changes-in-Diet-and-Lifestyle-and-Long-Term-Weight-Gain-in-Women-and-Men.pdf
3. Lloyd-Jones D, Adams RJ, Brown TM et al. Executive summary: Heart disease and stoke statistics – 2010 update: A report from the American Heart Association. Circulation 2010;121(7):948-954.
   http://circ.ahajournals.org/content/121/7/948.full.pdf

Do we really need nutritional supplements — and would they even do us any good? If we believe the naysayers, nutritional supplements like vitamins and minerals are worthless; no clinical vitamin/mineral trial has ever shown any benefit. Besides, we′re told, we can get all our vitamins and minerals from a balanced diet.

Relying on our diets for all our nutritional needs is simply unrealistic. There might well be such a thing as a "complete balanced diet", but survey after survey has shown that hardly anyone follows dietary recommendations. If you get all your necessary nutrients from the food you eat you are truly an exception.

Yet, there are nutrients that we simply can′t do without. We need vitamins, minerals, essential fatty acids and essential amino acids because we either cannot make them at all or cannot make them in adequate amounts. If we don′t get them from food and drink — and every nutrition survey shows that we don′t — where else could get them but from supplements? So, how could supplementation be found to be useless?

The reason why nutrient trials usually give disappointing results is that they employ tools designed to evaluate pharmaceutical drugs. But nutrients aren′t drugs, and methods like randomized controlled trials (RCTs) — the "gold standard" of medical research — simply aren′t suited to the assessment of nutritional supplements (1).

The crucial difference between nutrients and drugs is that drugs are foreign to the body. Drugs interfere in metabolism and are useful only when this interference halts or slows a disease process. Nutrients, on the other hand, support metabolic functions; supplements are taken to ensure an adequate supply of essential nutrients. Put differently, drugs are used to treat disease whereas nutritional supplements are taken to prevent disease and optimize health. This makes all the difference when assessing drugs and supplements.

In randomized placebo-controlled trials a substance is compared to a placebo (treatment versus control group). Control groups are readily available for drug trials since the drug doesn′t occur in nature. In contrast, everyone has some — usually sub-optimal — level of essential nutrients, i.e. there can be no genuine control group. It is impossible to carry out true placebo-controlled nutrient studies.

Drugs interfere in physiological processes and usually act quickly. Drug trials can therefore be completed in a reasonably short time, Nutritional deficiencies, on the other hand, may take years or even decades to lead to symptoms. Clinical trials of that length of time would be prohibitively expensive.

Clinical trials of single drugs make sense since every drug has an effect of its own. Nutrients, on the other hand, work together; all essential nutrients have to be present in adequate amounts for optimal health. Clinical trials of individual nutrients are pointless.

Of course, there are numerous other differences between drugs and nutritional supplements. Most importantly, drugs have dangerous side effects and need to be monitored carefully. Nutrients, on the other hand, have wide safety margins.

All this is obvious, yet large sums of money are squandered on studying nutrients with tools developed for drug evaluation — with predictably inconclusive results. It is almost as if these trials are meant to fail.

It is actually quite hypocritical to demand that nutritional recommendations be backed by randomized controlled trials; most pharmaceutical therapies aren′t based on RCTs either! First, many drugs are prescribed for off-label use. Secondly, most people on prescription drugs take more than one medication. Neither off-label nor multi-drug prescription is supported by the supposed medical "gold standard". A cynic might say that the concept of randomized controlled trials is mainly used to dismiss non-pharmaceutical therapies as unscientific".

Of course, nutritional recommendations should be based on scientific evidence. Just remember that it is not the need for nutrients that is in question, but rather the amounts that we need for optimal health. We may not know yet what those optimal nutrient levels are but, given today′s diets, most people will surely benefit from nutritional supplements.

Sources

1. Shao A, Mackay D, A commentary on the nutrient-chronic disease relationship and the new paradigm of evidence-based nutrition, Nat Med J 2010;2(12):10-18.
   http://www.naturalmedicinejournal.com/pdf/NMJ_DEC10_LR2.pdf

Do we really need nutritional supplements? Why couldn′t we get all the nutrients we need from a "balanced diet"? We probably could — if we ate right. But how many people eat right?

Apparently not too many. For example, there is a big gap between what Americans eat and the dietary recommendations outlined in Healthy People 2010. And things aren′t much better in other industrialized countries.

Healthy People 2010 recommends at least two daily servings of fruit, three servings of vegetables a third of which should be dark green or orange, and six servings of grains three of which should be whole grains. How closely did Americans follow this advice? National Health and Nutrition Examination Survey (NHANES) results showed (1) that in 2003 - 2004:

• only 40% of children and adults ate the recommended 2 servings of fruits per day
• only 7% of children and 11% of adults ate the recommened number of dark green or orange vegetables
• 54% of those surveyed ate the recommended number of servings of grains, but only 3% had 3 or more servings of whole grains

As scientists at the U.S. National Cancer Institute put it, "These findings add another piece to the rather disturbing picture that is emerging of a nation′s diet in crisis" (2).

State-run dietary surveys gave similarly dismal results (3). The 2007 data from the Behavioral Risk Factor Surveillance System (adults) and the Youth Risk Factor Surveillance System (grades 9 - 12) showed that:

• only 32.8% of adults and 32.2% of adolescents ate 2 or more fruits per day
• only 27.4% of adults and 13.2% of adolescents ate 3 or more vegetables
• only 14.0% of adults and 9.5% of adolescents ate both 2 or more fruits and 3 or more vegetables per day

Things hadn′t improved two years later. The 2009 surveys found that still only 32.5% of adults consumed 2 or more servings of fruits and only 26.3% of adults had 3 or more servings of vegetables per day (4).

Are the dietary recommendations set out in Healthy People 2010 too difficult to live up to? If anything, they may not go far enough; the food pyramid developed by scientists at the Harvard School of Public Health places even greater emphasis on eating fruits, vegetables, and whole grains (5).

The Harvard Food Pyramid was developed in response to the undue influence that the powerful food industry lobby exerts on government-issued dietary guidelines. The Harvard scheme doesn′t recommend serving sizes — it simply ranks different food groups according to their known health benefits. The pyramid consists of four layers which contain, from top (least healthy) to bottom (healthiest):

• butter, red and processed meat, refined grains, potatoes, sugary drinks and sweets
• dairy products
• nuts, seeds and tofu, and fish, poultry and eggs
• fruits and vegetables, whole grains, and healthy fats and oils

Of course, food pyramids aren′t just about micronutrients, but the failure to consume enough fruits, vegetables and whole grains is a clear indication that most of us don′t get enough vitamins and minerals from our diets. The authors of the Harvard Food Pyramid in fact acknowledge this and recommend a daily vitamin/mineral supplement for most people (5).

Sources

1. Healthy People 2010, Progress review — Nutrition and overweight presentation, 2008.
   http://www.cdc.gov/nchs/ppt/hp2010/focus_areas/fa19_2_ppt/fa19_nutrition2_ppt.htm
2. Krebs-Smith SM, Guenther PM, Subar AF et al, Americans do not meet federal dietary recommendations, J Nutr 2010;140(10):1832-1838.
   http://dx.doi.org/10.3945/jn.110.124826
3. CDC State indicator report on fruits and vegetables, 2009.
   http://www.fruitsandveggiesmatter.gov/downloads/StateIndicatorReport2009.pdf
4. State-specific trends in fruit and vegetable consumption among adults - United States, 2000 - 2009. Morbidity and Mortality Weekly Report, Centers for Disease Control and Prevention. 2010;59(35):1125-1130.
   http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5935a1.htm?s_cid=mm5935a1_w
5. Food pyramids: What should you really eat?
   http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/pyramid-full-story/index.html

P.S. I first published this article on Mike Adams′ NaturalNews site under the title "Americans lack nutrients because of poor eating choices". You can find all my NaturalNews pieces at http://naturalnews.com/author93.html.

Back to the battle of the bulge and the series of articles that got me going on that subject. The first part in the series focused on whether exercise would help you lose weight.

Here is how the author introduces the subject (1):

"It′s such a widely accepted idea it′s virtually dieting dogma, a belief pushed with almost religious zeal: You can′t lose weight without exercising more."

and

"We have been taught that exercise is a surefire path to weight loss. But controversy is growing over whether working out to lose weight can be an exercise in futility. At issue is whether the amount of exercise needed to make a meaningful impact is unrealistic and whether gluttony, and not sluggishness, is where we should be focusing our efforts."

So, does exercise help you lose weight? As the introduction implies, the answer seems to be no. This is also the conclusion of a 2009 Time Magazine article (2) that ruffled quite a few feathers. The author of that piece quotes an exercise expert as saying that "In general, for weight loss, exercise is pretty useless … The common belief that physical activity can counteract rising rates of obesity is based on a belief rather than on solid scientific evidence.".

Why doesn′t exercise lead to weight loss? The typical explanation is that people don′t work out long enough or intensely enough (1):

"The amount of exercise needed to cause significant weight loss is more than most free-living individuals are capable of undertaking, and that is particularly true for the obese".

"You need a lot of exercise, and a lot of time, to make a 200, 300, 400 calorie deficit whereas you can easily make a 1,000 calorie deficit by cutting down your intake "

Of course, not everyone agrees that exercising to lose weight is futile, even in the face of evidence to the contrary. Here is my favourite quote — it demonstrates so beautifully just how misguided expert advice can be (1):

"[It] makes no difference to the human body whether it sheds calories via eating less or exercising more. The end result is the same: weight is lost."

This statement is only partially right. It really doesn′t seem to matter whether we shed calories by eating less or exercising more; the result appears to be the same all right. Unfortunately, the outcome isn′t weight loss, but rather a failure to lose weight.

What is wrong with the idea that all you have to do is create an energy deficit and you′ll lose weight?

Suppose you are overweight or obese. If you′re not losing weight this has to mean that all your energy needs are met by the food you eat. You now start a regular exercise routine hoping to lose weight, i.e. to burn some of your stored fat. Question: Why should your exercise fuel come from your adipose tissue, when all your other metabolic needs are met by food?

For exercise to lead to weight loss it would have to do more than just create an energy deficit. Exercise would have to draw on the fat reserves stored in the body′s adipose tissue, without replenishing those stores afterwards.

Just because exercise doesn′t help you lose weight, this doesn′t mean it is useless. Physical activity has many health benefits, such as increased cardiovascular fitness and insulin sensitivity, lower blood pressure, and improved mental health and cognitive ability. It just doesn′t seem to help you lose weight.

Sources:

1. Sharon Kirkey. Exercise alone doesn′t cut it. Canwest News Service March 6, 2010.
   http://www.timescolonist.com/health/battle+cultural+epidemic/2660423/Exercise+alone+doesn/2649284/story.html
2. John Cloud. Why exercise won′t make you thin. Time Magazine August 9, 2009.
   http://www.time.com/time/printout/0,8816,1914857,00.html

The February 2011 issue of Scientific American ran an 8-page article on obesity which starts with this stark assessment of the situation:

"Obesity is a national health crisis — that much we know. If current trends continue, it will soon surpass smoking in the U.S. as the biggest single factor in early death, reduced quality of life and added health care costs … " (1)

That′s hardly an exaggeration. Obesity is a risk factor for cardiovascular disease and type 2 diabetes, two of the leading causes of premature death. In addition, the same lifestyle that leads to obesity also increases cancer risk. According to health experts from the Americal Institute for Cancer Research and the World Cancer Research Fund, simple lifestyle changes could prevent a third of all common cancers (2).

How did we ever get into this mess? By replacing real food and drink with processed junk. Not only is this stuff — you can′t call it nutrition — unhealthy but it is literally addictive (3). Food and drug abuse affect brain function in similar ways, and junk food eating patterns resemble drug addiction — binge eating, an inability to stop even though one is aware of adverse health consequences, an increase over time in the frequency and quantity of junk food eaten, etc. Small wonder then that the author of the SciAm article considers behaviour modification techniques developed for dealing with addiction to be society′s best hope for combatting the obesity epidemic:

"Behavior-focused studies of obesity and diets as early as the 1960s recognized some basic conditions that seemed correlated with a greater chance of losing weight and keeping it off: rigorously measuring and recording calories, exercise and weight; making modest, gradual changes rather than severe ones; eating balanced diets that go easy on fats and sugar rather than dropping major food groups; setting clear, modest goals; focusing on lifelong habits rather than short-term diets; and especially attending groups where dieters could receive encouragement to stick with their efforts and praise for having done so." (1)

Is this where we are headed? One of life′s most basic and pleasurable activities — eating — needs to be guided and supervised by behavioural psychologists, with therapy group meetings for reinforcement? We can′t seem to prevent the food processing industry from hooking us on their addictive junk, so we′ve created another industry, the weight loss industry complete with psychologists and therapy groups, to help us manage our addiction to the stuff.

Admittedly, some pressure is now being applied to the food industry to stop their nefarious business practices, but we still have a long way to go. Take the case of McDonald′s "Happy Meals". Apparently, the company gives away some cheap junk toy with every so-called Happy Meal. The kids want the toy and nag their parents until they get what they want. Clearly, McDonald′s manipulates parents through their children into buying junk food, and good luck to any parent trying to resist. This is about as blatant an example of manipulating children as you will find, yet there is opposition to banning the practice; such regulations are considered by many to be too intrusive (1).

We are in the grips of an ideology called capitalism, the naive belief that everyone′s selfish actions will automatically optimize the common good. This "invisible hand" may have worked in Adam Smith′s day, but it doesn′t work in this age of multinational corporations.

Power tends to corrupt; we have no trouble seeing this in the political arena. So why is it so difficult to recognize that economic power corrupts just as much, even in the face of the outrageous criminal behaviour of big multinational corporations in recent years. In fact, vested business interests arguably do more to corrupt the political process than political ambition. And this happens in broad daylight — it′s called lobbying.

Where does this naive belief in the automatic benefits of capitalism get us? A publicly traded company is expected to maximize financial returns for their share holders, but the company is perfectly free to sicken and kill those same share holders and their families with the junk they sell them in order to generate those financial returns.

Have we lost our way, or what?

Sources

1. David H. Freedman. How to fix the obesity crisis. Scientific American, February 2011.
2. Kate Kelland. Simple life changes could stop millions of cancers. Reuters, February 4, 2011.
3. Gearhard AN, Corbin WR, Brownell KD, Preliminary validation of the Yale Food Addiction Scale. Appetite (2009), doi:10.1016/j.appet.2008.12.003
   http://dx.doi.org/10.1016/j.appet.2008.12.003

Looking for a different Valentine′s Day treat this year? Create your own chocolate berry/fruit and nut clusters! They are easy to make and the ingredients — chocolate, dried fruits or berries, and nuts like almonds, cashews, pecans or hazelnuts — are inexpensive and readily available in the bulk food section of any supermarket. Make sure though you buy quality dark chocolate, preferably the semi -sweet variety. Try the following recipe — it′s simple and delicious:

Chocolate almond cranberry clusters

200 g    dark chocolate
75 g    almonds
75 g    dried cranberries

Cover a baking sheet with wax paper. Mix the nuts and berries. Heat the chocolate in a water bath and fold the berry/nut mixture into the melted chocolate, Grab a tea spoon, scoop out bite-size pieces of the mixture and drop them on the covered baking sheet; try to keep the clusters from touching. Refrigerate the whole thing for an hour or two and you have delicious chocolate almond cranberry clusters.

Appropriately enough for a Valentine′s treat, these chocolate clusters are actually quite heart-healthy — when consumed in moderation of course. All three ingredients contain polyphenolic and other antioxidants that have been shown to help reduce LDL oxidation, which in turn lowers the risk of atherosclerosis and cardiovascular disease. They contain many other important nutrients as well with additional health benefits. In fact, you′ll find nuts, berries, fruits, and even dark chocolate on every list of healthful snacks.

Use dried fruits like apricots, pineapples, papayas or prunes instead of cranberries. Try pecans, cashews, or hazelnuts instead of almonds. Use your imagination. Experiment!

Enjoy!

How close are we to genetic medicine?

A couple of posts ago ("The future of medicine, and other fantasies") I commented on a recent Scientific American article on the future of medicine (1). The author of the piece focused on the promises of stem cell research and potential payoffs from the genome project. I share his hopes for medical breakthroughs from stem cell research, but I find his take on genomic medicine rather naive:

“[The] one-size-fits-all medicine we have seen for the past 100 years will yield to medicine tailored to each individual. Doctors will prescribe a custom prevention program and make comprehensive diagnoses according to each patient′s genes, bacteria, allergens, fungi, viruses and immune system.

Studying the specific combinations of genes and environmental factors can lead to changes in diet, drugs and behavior, helping us extend our healthy years.

Your genome will get sequenced every year or so to check for the emergence of cancer cells, autoimmune cells, inflammation, and so on and will help predict what treatment may work best if a disease appears” (1)

What′s so improbable about this scenario? It ignores the causal role of the food and drug industries in our health crisis. How do you develop custom prevention programs, improve diet, and change behaviour while food companies do everything in their power to peddle junk food and drug companies maintain an iron grip on the medical profession and their "healing" monopoly?

The authors of two recent articles on the promise of genome-wide association studies (GWASs) — the prediction of disease risk from the patterns of genetic mutations — are a good deal more realistic in their assessment of the promise of genetic medicine (2,3). They point out that so far genome-wide screening has neither lived up to expectations nor is it clear that it would be cost-effective.

Genome-wide screening has identified a number of alleles (gene variants) associated with various diseases, but to date no major susceptibility alleles have been found; each of the known risk-associated alleles has at most a small effect on disease risk. Even their combination accounts for only a small percentage of known genetic risk variations, likely because the relationship between genetic variation and environment is as yet poorly understood:

"What is becoming clear from these early attempts at genetically based risk assessment is that currently known variants explain too little about the risk of disease occurrence to be of clinically useful predictive value." (2)

Even if GWASs led to reliable predictors of disease risk, population-wide screening would hardly be justified; medical expenses already threaten to bankrupt most industrialized countries. Screening everyone would at best identify those who are genetically predisposed to develop a certain disease but have no family history of that disease. Even then genetic screening would only be worthwhile if saving lives depended on identifying and treating individuals at risk before clinical symptoms appeared.

Genetic risk factors only predispose to disease; actual disease development depends on gene-environment interactions. Prevention would therefore mostly consist of lifestyle changes like smoking cessation, dietary improvements, and exercise. It is questionable whether the threat of a possible future illness will motivate people to make the necessary changes; and without implementing preventive measures genetic screening is pointless:

"Before genetic information is used in public health screening, it must be shown that:

• such information predicts disease risk better than phenotypic information;
• cost-effective interventions exist for those at increased genetic risk;
• these interventions are more cost-effective than population-level interventions;
• genetic risk information motivates desired behaviour change.

Currently there are no examples of genetic screening for disease risk that satisfy these criteria." (3)

Sequencing the human genome was a major scientific achievement, but we are unlikely to derive significant health benefits from it. Population-wide lifestyle changes offer by far the greatest potential pay-off, and for that you don′t need your genome sequenced. Healthy living is a good idea for everyone, regardless of genetic make-up.

Sources:

1. Church G. Medicine I can call my own. In What comes next: Experts predict the future. Scientific American September 2010.
   http://www.scientificamerican.com/article.cfm?id=what-comes-next&page=5
2. Feero WG, Guttmacher AE. Genomewide association studies and assessment of the risk of disease. New Engl J Med 2010;363(2):166-176.
   http://content.nejm.org/cgi/reprint/363/2/166.pdf
3. Hall WD, Mathews R, Morley KI. Being more realistic about the public health impact of genomic medicine. PLoS Medicine 2010;7(10):e1000347.
   http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.1000347