Yogurt increases weight loss
August 1, 2009
From The International Journal of Obesity:
BACKGROUND AND OBJECTIVE: We have previously demonstrated an antiobesity effect of dietary Ca; this is largely mediated by Ca suppression of calcitriol levels, resulting in reduced adipocyte intracellular Ca2+ and, consequently, a coordinated increase in lipid utilization and decrease in lipogenesis. Notably, dairy Ca is markedly more effective than other Ca sources.
DESIGN: Obese subjects were placed on balanced deficit (-500 kcal/day) diets and randomized to control (400–500 mg Ca/day; n=16) or yogurt (1100 mg Ca/day; n=18) treatments for 12 weeks. Dietary macronutrients and fiber were held constant at the US average.
MEASUREMENTS: Body weight, body fat and fat distribution (by dual-energy X-ray absorptiometry), blood pressure and circulating lipids were measured at baseline and after 12 weeks of intervention.
RESULTS: Fat loss was markedly increased on the yogurt diet (-4.43plusminus0.47 vs -2.75plusminus0.73 kg in yogurt and control groups; P<0.005) while lean tissue loss was reduced by 31% on the yogurt diet. Trunk fat loss was augmented by 81% on the yogurt vs control diet (P<0.001), and this was reflected in a markedly greater reduction in waist circumference (-3.99plusminus0.48 vs -0.58plusminus1.04 cm, P<0.001). Further, the fraction of fat lost from the trunk was higher on the yogurt diet vs control (P<0.005).
CONCLUSION: Isocaloric substitution of yogurt for other foods significantly augments fat loss and reduces central adiposity during energy restriction.
Top Science Journals
July 21, 2009
13,000 Phage Generations: An Arms race
July 18, 2009
The abstract:
Bacteriophage {phi}X174 was evolved on a continuous supply of sensitive hosts for 180 days (~13,000 phage generations). The average rate of nucleotide substitution was nearly 0.2% (11 substitutions)/20 days, and, surprisingly, substitutions accumulated in a clock-like manner throughout the study, except for a low rate during the first 20 days. Rates of silent and missense substitutions varied over time and among genes. Approximately 40% of the 71 missense changes and 25% of the 58 silent changes have been observed in previous adaptations; the rate of parallel substitution was highest in the early phase of the evolution, but 7% of the later changes had evolved in previous studies of much shorter duration. Several lines of evidence suggest that most of the changes were adaptive, even many of the silent substitutions. The sustained, high rate of adaptive evolution for 180 days defies a model of adaptation to a constant environment. We instead suggest that continuing molecular evolution reflects a potentially indefinite arms race, stemming from high levels of co-infection and the resulting conflict among genomes competing within the same cell.
Diets that promote oxidative stress favor impairment in glucose homeostasis. In this context, increasing the cysteine intake may be beneficial by maintaining glutathione status. We have investigated the effects of dietary cysteine on oxidative stress and glucose homeostasis in rats fed a high-sucrose (HS) diet. Rats were assigned for 6 weeks to a standard diet or to HS diets in which the protein source was either an alpha-lactalbumin-rich whey concentrate (a cysteine-rich protein) or the total milk proteins alone or supplemented with 5.8 or 20 g N-acetylcysteine per kilogram of food. Increasing the cysteine intake prevented HS-induced oxidative stress, as assessed by blood and tissue glutathione and carbonyl levels. At the same time, the HS-induced glucose intolerance, impaired postprandial glycemic control, and decrease in muscle and liver insulin-induced activation of insulin receptor substrate 1 and Akt were prevented by increasing the level of dietary cysteine, a major original finding. Of great interest was the observation that all beneficial effects of cysteine supplementation were duplicated by the consumption of a cysteine-rich protein. These data show that increasing the cysteine intake limits HS-induced impairment of glucose homeostasis and suggest that these effects are mediated by a reduction in oxidative stress.
The paper suggests, along with many other studies, that a cysteine-rich protein diet can alleviate oxidative stress in aging. To the extent that aging just is oxidative stress, that means that aging could be susceptible to a simple means of combating it.
A Cause of the Secular Decline in Violence
July 17, 2009
Steven Pinker writes on the well-known (in the Steveosphere) decline in violence from the Middle Ages to today, and suggests four possible reasons for the decline: wider governmental control, a sense that life is no longer cheap (from better sanitary and medical conditions etc.), greater incentives to cooperate, and an escalation in empathy, (Singer’s “expanding moral circle”).
He doesn’t mention another and nearly proven possibility: evolution. Clark showed convincingly that England’s population evolved over several hundred years up to 1800, with middle class personality traits increasing in incidence among the population. Cochran and Harpending have shown convincingly that evolution currently proceeds at a rate up to 100 times faster than before civilization; furthermore, they asserted that the breeding of docility is a process that civilization could be expected to encourage, so it would also be likely from living under expanded and more powerful governments.
Pinker writes:
Whatever its causes, the decline of violence has profound implications. It is not a license for complacency: We enjoy the peace we find today because people in past generations were appalled by the violence in their time and worked to end it, and so we should work to end the appalling violence in our time.
Not necessarily, Dr. Pinker. Or if they did work to end it, some of their methods included the massive application of capital punishment and letting the poor starve, along with other measures that few would advocate today.
Awhile back I noted a paper which showed that vitamin C abolished endurance training effects. It turns out that vitamin C isn’t the only substance that will do this: Antioxidants prevent health-promoting effects of physical exercise in humans. This from the PNAS, a high-impact journal; this study isn’t shoddy work, in other words.
The experimenters took two groups of young men, previously trained with endurance exercise, and previously untrained. Each group in turn was randomized to receive antioxidant supplements in the form of 400 IU vitamin E and 1000 mg vitamin C daily, or placebos. Then the men underwent 4 weeks of training, 5 days a week, including biking, running, and circuit training.
The result: those who had taken antioxidants saw no, repeat, no health benefits from exercise. The measurements done were of insulin sensitivity, TBARS (a measure of oxidative stress), and several others. In each of them, those who exercised, and did not take antioxidants, regardless of whether they had trained previously or not, saw an increase in insulin sensitivity, a decrease in TBARS, and so on, while these effects were abolished in those who took the antioxidants. Further, the promotion of muscle antioxidant defenses which is normally promoted by exercise was prevented by supplementation.
From the paper:
Most importantly, these changes in gene expression and the increase in insulin sensitivity following physical exercise are almost completely abrogated by daily ingestion of the commonly used antioxidants vitamin C and vitamin E. Thus, antioxidant supplementation blocks many of the beneficial effects of exercise on metabolism.
What are the larger implications here? What about that high fruit and vegetable intake that we are constantly told is so good for us? this is where it gets very interesting:
If transient increases in oxidative stress are capable of counteracting insulin resistance in humans, it is possible that preventing the formation of ROS by, for example, antioxidants might actually increase, rather than decrease, the risk of type 2 diabetes. While this remains to be determined, one metaanalysis of previously published studies (27) suggests that high dietary intake of fruits and vegetables, a source of antioxidants but also of numerous other bio-active compounds, may actually decrease the risk for type 2 diabetes. Nevertheless, and as stated by Hamer and Chida (27), all larger intervention trials evaluating the diabetes-preventive potential of defined antioxidant supplements have been unable to find any positive effects of supplementation (28–30). Moreover, antioxidant use in type 2 diabetics has been linked to increased prevalence of hypertension (31) and use of antioxidant supplements has recently been proposed to increase overall mortality in the general population (32). Taken together, these previously published findings tentatively suggest that fruits and vegetables may exert health-promoting effects despite their antioxidant content and possibly due to other bio-active compounds. [...]
Free radicals causing oxidative stress are an inevitable by-product of mitochondrial metabolism and have been proposed to exert repetitive damage to individual cells of the body promoting increased disease prevalence and aging (33). However, and in specific regard to exercise, antioxidants were incapable of further extending exercise-induced lifespan extension in rats (26). Repeated exposure to sublethal stress has been proposed to cumulate in enhanced stress resistance and ultimately increased survival rates due to a process named hormesis. By analogy, for sublethal ROS-dependent processes emanating from the mitochondria, the term “mitohormesis” was recently proposed on a hypothetical basis (34). Evidence for this novel concept has been provided in model organisms such as nematodes (15) and rats (17), and the current study would extend the concept of mitohormesis to the amelioration of insulin resistance in humans, suggesting that potential harmful ROS may exert health promoting effects via defined molecular intermediates (Fig. 3). [...]
Taken together, we find that antioxidant supplements prevent the induction of molecular regulators of insulin sensitivity and endogenous antioxidant defense by physical exercise. Consistent with the concept of mitohormesis, we propose that transiently increased levels of oxidative stress reflect a potentially health-promoting process at least in regards to prevention of insulin resistance and type 2 diabetes mellitus. [My emphases.]
Reference was made above to nematodes, in this case the famous Caenorhabditis elegans, the subject of Cynthia Kenyon’s longevity experiments. In the study referenced above:
Reduced glucose availability promotes formation of reactive oxygen species (ROS), induces catalase activity, and increases oxidative stress resistance and survival rates, altogether providing direct evidence for a hitherto hypothetical concept named mitochondrial hormesis or “mitohormesis.” Accordingly, treatment of nematodes with different antioxidants and vitamins prevents extension of life span. In summary, these data indicate that glucose restriction promotes mitochondrial metabolism, causing increased ROS formation and cumulating in hormetic extension of life span, questioning current treatments of type 2 diabetes as well as the widespread use of antioxidant supplements. [Link.]
My takeaway on all this: low carb diets promote health and longevity by, among other things but perhaps mainly, increasing insulin sensitivity, and along with it, decreasing inflammation. This is the lesson from Kenyon’s worm experiments, in which insulin signaling is disrupted, causing the worms to have up to a 6-fold increase in longevity. But antioxidants appear to completely abolish this activity related to insulin signaling.
There have been many arguments on both sides of the antioxidant debate, but this one I find very convincing, enough so that it appears that antioxidants are bad for your health.
These are some notes I’ve collected which I place here while collecting my thoughts to write something longer.
Most will be familiar with the phenomenon of calorie restriction (CR) and the fact that it dramatically increases both mean and maximum lifespan in many different species of animals, from yeast to mammals.
It turns out that CR usually also amounts to protein restriction, and that is the true driver of the CR effect on longevity. Furthermore, recent research has determined that the restriction of only one amino acid is responsible for the increasing longevity seen in CR, and that is methionine. See this abstract for an explanation. (Interesting to note that a great deal of this work has been done in Spain, ranked 9th in the world in scientific output.)
Methionine restriction works through several pathways, such as increasing insulin sensitivity, decreasing visceral fat, and lowering IGF-1 levels, as well as decreasing the production of oxygen radicals by mitochondria. Methionine restriction also increases blood glutathione levels – that’s a good thing.
A number of humans are attempting calorie restriction; however, it appears that until now they’ve been blowing it, at least partially, because they increased their protein intake, or didn’t change it, and while they have received benefits in the form of lower blood pressure and better cardiovascular disease markers, their serum IGF-1 levels did not decrease, thus denying them full benefits. But (same paper), when protein levels were restricted, IGF-1 levels plummeted within weeks.
All this is interesting because calorie restriction, though it might bring huge health benefits for humans, is something that only highly disciplined people can carry out. But restricting protein ought to be pretty easy – no need to go hungry.
Which diet is lowest in protein? Score one for the vegans. (That’s from my favorite journal.)
On the other hand, it’s pretty clear that restricting carbohydrates in the diet is also a good strategy for health, and vegans usually have a high carb intake. (CR research has shown that neither carbohydrate restriction nor fat restriction is responsible for CR longevity effects.) It seems that a good strategy for those desiring to pursue both protein and carbohydrate restriction might be the Kwasniewski or “Optimal” diet.
From an evolutionary point of view, it’s thought that CR works because in conditions of food scarcity, it allows an animal to “survive and fight another day”. Methionine, the protein constituent which appears to be the driver of CR, is an essential amino acid in humans, found most abundantly in meat. Methionine scarcity – and I’m speculating here – appears to be an indication of scarcity in general; it would be the first dietary element to disappear when conditions of scarcity begin; so it makes sense that its restriction causes CR longevity effects.
