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mcsblues
07-16-2006, 09:41 PM
Sounds like low carb right? - and to be sure, a better macronutrient profile would doubtless be even more effective at controlling insulin ... and LEF do just happen to sell pinolenic acid (pine nut extract) ... anyone for pesto? ;) - but it is still an interesting article! :D

Calorie Restriction without Hunger!

By Steven V. Joyal, MD, and Dale Kiefer

People today are missing out on a tremendous opportunity to achieve a radically extended healthy life span, along with significant reductions in body fat.

In a study just published in the Journal of the American Medical Association, the effects of caloric restriction were measured in a group of overweight adults over a six-month period.1 The findings were nothing short of astounding!

In response to reduced food intake, fasting insulin levels plummeted. As Life Extension members learned long ago, excess insulin functions as a death hormone that devastates virtually every cell and organ system in the body.

Insulin overload increases the risk of heart disease, cancer, blindness, stroke, Alzheimer’s, and other age-related diseases.2-6

The most exciting finding of this study was the amount of weight lost in the groups that restricted their calorie intake. The moderate caloric-restriction group experienced a 24% reduction in body fat mass, while the very low-calorie group achieved a 32% reduction in fat mass.1

You may be wondering how these findings pertain to you, since hunger is the factor that precludes most people from even considering a low-calorie diet.

The remarkable news is that pinolenic acid—a natural plant extract discovered in Europe—has been shown to suppress appetite dramatically without causing any stimulatory effect. This plant extract attacks the underlying mechanisms involved in hunger so effectively that study participants reduced their food intake by 36%.7

Aging adults too often suffer from the pathological effects of insulin overload and excess fat mass. This natural appetite-suppressing nutrient could help great numbers of people enjoy the multiple health benefits documented in the recent Journal of the American Medical Association study. These benefits include reduced DNA damage, along with significant reductions in fasting insulin, total body weight, and fat mass.1

An increasing body of scientific findings reveals that excess serum insulin, also known as hyper-insulinemia, is a major health problem. High serum insulin promotes high blood pressure by impairing sodium balance.4,8 Prolonged exposure to excess insulin can severely compromise the vascular system.4,8 By acting as a catalyst in promoting cell growth, excess insulin also increases the risk for and progression of certain cancers.3 High insulin promotes the formation of beta-amyloid in brain cells and may contribute to the development of Alzheimer’s disease.5 Overproduction of insulin even contributes to prostate enlargement by helping to promote the overgrowth of prostate cells.9 Insulin resistance is associated with the development of abdominal obesity and health problems such as atherosclerosis and impotence. Furthermore, insulin resistance and obesity are risk factors for type II diabetes.4 Excess insulin (hyper-insulinemia) is predictive for type II diabetes mellitus.10

Perhaps the simplest way to evaluate the toxic effects of excess insulin is to look at its effects on human mortality. One study showed that over a 10-year period, the risk of dying was almost twice as great for those with the highest insulin levels than for those with the lowest levels. The study authors stated that hyperinsulinemia is associated with increased all-cause and cardiovascular mortality independent of other risk factors.6

Decreasing excess insulin by enhancing insulin sensitivity and improving the function of pancreatic beta cells (the cells that produce insulin in the body) is a crucial component in the quest for longevity. The best way to lower excess insulin levels is to eat less and lose weight.

Multiple Health Dangers of Excess Fat

As fat accumulates, it releases free fatty acids into the bloodstream, a process that promotes insulin resistance.11 As cells lose their ability to respond to insulin efficiently, insulin levels rise. Insulin serves to shepherd glucose molecules from the bloodstream across cell membranes and into cells, where the sugar molecules are metabolized for energy. As insulin resistance mounts, the body attempts to compensate by pumping out ever higher amounts of insulin. Meanwhile, excess glucose in the bloodstream—a condition known as hyperglycemia—damages blood vessels and nerves, and may eventually cause problems throughout the body.12,13

In the past, fat cells were considered metabolic “dead weight,” so to speak—inactive and unimportant to metabolism. Life Extension members have known for several years that nothing could be further from the truth.Fat cells (adipose tissue) release fatty acids and generate proteins and hormones that are associated with potentially deadly inflammation.14,15 At the current time, scientists have identified more than 100 proteins, fatty acids, hormones, and inflammatory agents that are secreted by fat cells.16

As fat accumulates, especially in the abdominal area, insulin sensitivity and glucose tolerance worsen. Left unchecked, this can lead to type II diabetes and a host of other diseases, including high blood pressure, elevated blood lipids such as triglycerides and low-density lipoprotein (LDL), and sky-high insulin levels.

The combination of insulin resistance leading to high blood pressure, abnormal cholesterol levels, abdominal obesity, and high blood sugar (glucose) is known as metabolic syndrome.17,18 Elevated cholesterol and high blood pressure also contribute to the development of endothelial dysfunction, a critical step in the development of atherosclerosis and cardiovascular disease.

One of the most effective ways to fight the scourge of deadly insulin resistance and obesity is caloric restriction, the practice of voluntarily decreasing calorie intake while maintaining good nutritional status. This is the same strategy shown to radically extend life span in lower animals and primates. A number of human studies are ongoing to validate the effects of caloric restriction in human longevity.

The greatest obstacle faced by anyone undertaking caloric restriction and trying to achieve sustained weight reduction is the nagging sensation of feeling hungry. Most people give in to this craving and thus forgo the opportunity to reduce their risks for life-threatening diseases. Fortunately, pinolenic acid, a newly discovered phytonutrient from the Korean pine nut, increases food satisfaction and food fullness by encouraging the secretion of hormones in the gut that are intimately involved in appetite control.

How Satiety Hormones Affect Appetite

Satiety is the sense of food satisfaction and fullness experienced after eating. Hunger and satiety both depend on a complex feedback loop involving many hormones and other substances secreted by the gut that interact with control centers in the brain. The gut participates in the hunger-satiety circuit by secreting two important hormones, cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), among others.
Cholecystokinin is recognized to suppress appetite in humans. When a partially digested meal rich in fats or proteins leaves the stomach to enter the duodenum (the first portion of the small intestine), the duodenal mucosa cells secrete CCK. In turn, CCK stimulates the pancreas to secrete numerous enzymes to help digest food. CCK also acts on the gallbladder to stimulate the release of bile into the small intestine, which helps to emulsify and break down fats. Most important to appetite control, CCK acts to slow gastric emptying and to promote a feeling of fullness, thus suppressing further food intake.19

Glucagon-like peptide-1 is another hormone that is intimately connected with fullness and satiety. Produced in the small intestine in response to fat and carbohydrates, GLP-1 works in part by activating the “ileal brake” mechanism. This slows down the absorption of food in the gut, promoting feelings of fullness and satiety, and therefore limits the desire for further food intake.20

GLP-1 also helps to control the health of pancreatic beta cells, which serve the crucial function of manufacturing insulin in the body. Abnormal beta-cell function plays a key role in the development of insulin resistance, and scientists believe that therapies that boost GLP-1 levels could help to favorably alter the course of diabetes.21

CCK and GLP-1 are key hormones for appetite control and satiety, and scientific studies show that these two hormones exert effects in combination that are more powerful than either alone (synergistic effects).15,22-27 Studies of normal-weight and obese subjects have shown that GLP-1 and CCK reduce feelings of hunger and decrease voluntary food intake at meals.28-31

Recent findings demonstrate that pinolenic acid, a polyunsaturated fatty acid derived from pine nuts, stimulates the secretion of the hunger-suppressing hormones CCK and GLP-1.7 This exciting finding suggests that pinolenic acid may have powerful effects in reducing appetite and increasing food satisfaction and fullness.

Pinolenic Acid: Effective Appetite Suppressant

In early 2006, scientists reported on the health benefits of Korean pine nut extract at a meeting of the American Chemical Society.
They described the results of a randomized, double-blind, placebo-controlled trial to determine how supplementing with pine nut-derived pinolenic acid affected feelings of satiety and hunger.7 The researchers discovered that the pine-nut extract stimulates production of the two important hunger suppressing hormones CCK and GLP-1.
In this study, overweight women were given either 3 grams of pinolenic acid or inactive placebo (olive oil) immediately before eating a modest breakfast consisting of carbohydrates. Scientists drew blood and measured for hormones associated with hunger, satiety, and eating behavior, at baseline and thereafter at regular intervals for four hours following the initial dose. The women also provided assessments of their perceived hunger at each interval.7

The women were asked to rate their “desire to eat” and “prospective food intake.” Those who received pinolenic acid reported significantly decreased hunger compared to subjects who had taken placebo. Subjects who received pinolenic acid rated their “desire to eat” an impressive 29% lower than placebo subjects, while they rated their “prospective food intake” 36% lower than those who received placebo.7

Furthermore, the lab tests in this study showed that pinolenic acid increased satiety hormones like CCK in the participants’ bloodstreams.7 Specifically, four hours after taking pinolenic acid, test subjects had 60% more CCK circulating in their bloodstreams than did placebo subjects.7
Among the pinolenic acid subjects, levels of GLP-1 initially climbed in both the placebo and pinolenic acid subjects. In the placebo group, however, GLP-1 values began to drop after 30 minutes and continued to decline steadily for the remainder of the four-hour test period. In the women supplemented with pinolenic acid, GLP-1 levels continued to rise, peaking at one hour and reaching a level well above that achieved by placebo subjects. GLP-1 levels remained comfortably above those of placebo subjects throughout the trial, peaking again at three hours post-dose, and this time achieving an even greater increase in levels of this satiety-enhancing hormone over placebo subjects. In total, over four hours, GLP-1 increased 25% more in subjects who took pinolenic acid than in those who took the placebo.7

The benefit of appetite control at mealtime is critical to anyone interested in cutting calories and losing weight, especially those who have struggled to overcome feelings of hunger and deprivation while dieting. Pinolenic acid, a natural fatty acid derived from the Korean pine nut, offers an effective tool to help enhance satiety and appetite control.
Promoting satiety and thus curbing the impulse to over-indulge at mealtime is just one of the beneficial effects of pinolenic acid. Recent research has demonstrated that when subjects are given GLP-1 before a meal, their blood sugar remains lower and their blood cholesterol levels are reduced compared to subjects given placebo. Since elevated blood sugar and high cholesterol after meals are associated with diabetes and cardiovascular disease, researchers speculate that therapies that boost GLP-1 levels (such as pinolenic acid) may be helpful in preventing cardiovascular disease.32

In another study, Japanese researchers fed pinolenic acid to animals bred to develop high blood pressure, a known risk factor for cardiovascular diseases like stroke and heart attack. After five weeks of feeding, the animals’ blood pressure readings were substantially lowered. Decreased cholesterol levels also were noted in the pinolenic acid-fed animals.33

Scientists have investigated the mechanism by which pinolenic acid lowers cholesterol. They found that after adding concentrated pinolenic acid extracted from pine nuts, enhanced uptake of detrimental LDL by liver cells was observed. The scientists suggest that the pinolenic acid concentrate may have LDL-lowering properties by enhancing liver LDL uptake.34

Health Benefits of Caloric Restriction

By suppressing appetite, pino-lenic acid may contribute to a successful caloric-restriction regimen. Scientific studies continue to confirm the life span-enhancing, disease-preventive benefits of caloric restriction. If you are not overweight but are interested in limiting your calorie intake to promote longevity and reduce disease risk, pinolenic acid can help enhance satiety and control appetite, critical factors involved in decreasing calorie intake.

In a recent study reported in the Journal of the American Medical Association (JAMA), subjects were put on calorie-restricted diets for six months, after which they were assessed for known markers of aging, such as core body temperature and levels of glucose, fasting insulin, and dehydroepiandrosterone sulfate (DHEA-S). Fasting insulin levels were significantly reduced in all the treatment groups, while DHEA-S and glucose (blood sugar) levels remained steady. On average, body weight decreased by 10% in the calorie-restriction and calorie-restriction-with-exercise groups, while body fat decreased by 24-25%. The subjects on a very low-calorie diet lost 13.9% of their initial body weight and 32% of their body fat. By contrast, body weight remained virtually unchanged in the control subjects.1

Core body temperature also fell in the calorie-restriction and calorie-restriction-with-exercise groups. Absolute 24-hour energy expenditure and sleeping energy expenditure decreased in all treatment groups, and the effect was more than could be explained by changes in body composition (fat loss). The researchers concluded that caloric restriction induced a “metabolic adaptation”—that is, a reduction in the baseline rate at which the body burns fuel. This adaptation is desirable for the purpose of slowing aging. People seeking to improve fitness and lose weight often exercise vigorously in the hope that exercise will boost their metabolic rate. While this may burn calories slightly more rapidly, it also accelerates the production of dangerous free radicals. According to a prevailing theory of aging, oxidative damage at the level of the mitochondria is responsible for much of the inflammation and degeneration associated with aging.1

In the JAMA study, DNA damage decreased from baseline levels in all the calorie-restricted groups. Accumulating DNA damage is thought to contribute to aging and disease processes such as cancer. This provides further evidence of the potentially life-extending effects of caloric restriction. In just six months, caloric restriction favorably altered fasting insulin levels and reduced core body temperatures in all treatment groups. Fasting insulin level and body core temperature are considered biomarkers for longevity. Taken together, the changes in longevity parameters among all calorie-restriction groups suggest that long-term caloric restriction may extend life span.1 Conversely, mounting evidence suggests that excess fat (what scientists call “adiposity”) is associated with accelerated aging.2

Conclusion

Although a reliable method of increasing longevity in countless scientific studies, caloric restriction is very difficult on a practical level over the long term, due in large part to sensations of hunger and food deprivation. Furthermore, given the well-known health dangers associated with excess body weight and fat, successful weight loss may literally be a matter of life and death for many overweight people.

Pinolenic acid from the Korean pine nut is a safe, effective nutritional supplement that can help overweight, aging adults by increasing feelings of food satisfaction and fullness. By stimulating the release of satiety and appetite-control hormones like CCK and GLP-1, pinolenic acid supplementation can suppress the feelings of gnawing hunger and deprivation that may sabotage weight-loss efforts.

References

1. Heilbronn LK, de JL, Frisard MI, et al. Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial. JAMA. 2006 Apr 5;295(13):1539-48.
2. Fontana L. Excessive adiposity, calorie restriction, and aging. JAMA. 2006 Apr 5;295(13):1577-8.
3. Calle EE, Kaaks R. Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nat Rev Cancer. 2004 Aug;4( 8 ):579-91.
4. Lakka HM, Laaksonen DE, Lakka TA, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA. 2002 Dec 4;288(21):2709-16.
5. Messier C, Teutenberg K. The role of insulin, insulin growth factor, and insulin-degrading enzyme in brain aging and Alzheimer’s disease. Neural Plast. 2005;12(4):311-28.
6. Dekker JM, Girman C, Rhodes T, et al. Metabolic syndrome and 10-year cardio-vascular disease risk in the Hoorn Study. Circulation. 2005 Aug 2;112(5):666-73.
7. Causey JL. Korean pine nut fatty acids induce satiety-producing hormone release in overweight human volunteers. Paper presented at: American Chemical Society National Meeting & Exposition; March 26-30, 2006; Atlanta, GA..
8. Manrique C, Lastra G, Whaley-Connell A, Sowers JR. Hypertension and the cardiometabolic syndrome. J Clin Hypertens. 2005 Aug;7( 8 ):471-6.
9. Amling CL. Relationship between obesity and prostate cancer. Curr Opin Urol. 2005 May;15(3):167-71.
10. Haffner SM. Risk constellations in patients with the metabolic syndrome: epidemiology, diagnosis, and treatment patterns. Am J Med. 2006 May;119(5 Suppl 1):S3-9.
11. Capeau J. Insulin signaling: mechanisms altered in insulin resistance. Med Sci (Paris). 2005 Dec;21 Spec No:34-9.
12. Home P. Contributions of basal and post-prandial hyperglycaemia to micro- and macrovascular complications in people with type 2 diabetes. Curr Med Res Opin. 2005 Jul;21(7):989-98.
13. Ardigo D, Valtuena S, Zavaroni I, Baroni MC, Delsignore R. Pulmonary complications in diabetes mellitus: the role of glycemic control. Curr Drug Targets Inflamm Allergy. 2004 Dec;3(4):455-8.
14. Lacquemant C, Vasseur F, Lepretre F, Froguel P. Adipocytokins, obesity and development of type 2 diabetes. Med Sci (Paris). 2005 Dec;21 Spec No10-8.
15. Trayhurn P. Endocrine and signalling role of adipose tissue: new perspectives on fat. Acta Physiol Scand. 2005 Aug;184(4):285-93.
16. Hauner H. Secretory factors from human adipose tissue and their functional role. Proc Nutr Soc. 2005 May;64(2):163-9.
17. Bhansali A, Dutta P. Pathophysiology of prediabetes. J Indian Med Assoc. 2005 Nov;103(11):594-5.
18. Petersen KF, Shulman GI. Etiology of insulin resistance. Am J Med. 2006 May;119(5 Suppl 1):S10-6.
19. Little TJ, Horowitz M, Feinle-Bisset C. Role of cholecystokinin in appetite control and body weight regulation. Obes Rev. 2005 Nov;6(4):297-306.
20. Verdich C, Flint A, Gutzwiller JP, et al. A meta-analysis of the effect of glucagon-like peptide-1 (7-36) amide on ad libitum energy intake in humans. J Clin Endocrinol Metab. 2001 Sep;86(9):4382-9.
21. Stoffers DA. The development of beta-cell mass: recent progress and potential role of GLP-1. Horm Metab Res. 2004 Nov-Dec;36(11-12):811-21.
22. Paquot N, Tappy L. Adipocytokines: link between obesity, type 2 diabetes and atherosclerosis. Rev Med Liege. 2005 May;60(5-6):369-73.
23. Christophe J. Is there appetite after GLP-1 and PACAP? Ann NY Acad Sci. 1998 Dec 11;865:323-35.
24. Flint A, Raben A, Astrup A, Holst JJ. Glucagon-like peptide 1 promotes satiety and suppresses energy intake in humans. J Clin Invest. 1998 Feb 1;101(3):515-20.
25. Gutzwiller JP, Degen L, Matzinger D, Prestin S, Beglinger C. Interaction between GLP-1 and CCK-33 in inhibiting food intake and appetite in men. Am J Physiol Regul Integr Comp Physiol. 2004 Sep;287(3):R562-7.
26. Marx J. Cellular warriors at the battle of the bulge. Science. 2003 Feb 7;299(5608):846-9.
27. Brennan IM, Feltrin KL, Horowitz M, et al. Evaluation of interactions between CCK and GLP-1 in their effects on appetite, energy intake, and antropyloroduodenal motility in healthy men. Am J Physiol Regul Integr Comp Physiol. 2005 Jun;288(6):R1477-85.
28. Naslund E, Barkeling B, King N, et al. Energy intake and appetite are suppressed by glucagon-like peptide-1 (GLP-1) in obese men. Int J Obes Relat Metab Disord. 1999 Mar;23(3):304-11.
29. Schick RR, Schusdziarra V, Mossner J, et al. Effect of CCK on food intake in man: physiological or pharmacological effect? Z Gastroenterol. 1991 Feb;29(2):53-8.
30. Adam TC, Westerterp-Plantenga MS. Glucagon-like peptide-1 release and satiety after a nutrient challenge in normal-weight and obese subjects. Br J Nutr. 2005 Jun;93(6):845-51.
31. Lieverse RJ, Jansen JB, Masclee AA, Lamers CB. Satiety effects of a physiological dose of cholecystokinin in humans. Gut. 1995 Feb;36(2):176-9.
32. Meier JJ, Gethmann A, Gotze O, et al. Glucagon-like peptide 1 abolishes the postprandial rise in triglyceride concentrations and lowers levels of non-esterified fatty acids in humans. Diabetologia. 2006 Mar;49(3):452-8.
33. Sugano M, Ikeda I, Wakamatsu K, Oka T. Influence of Korean pine (Pinus koraiensis)-seed oil containing cis-5,cis-9,cis-12-octadecatrienoic acid on polyunsaturated fatty acid metabolism, eicosanoid production and blood pressure of rats. Br J Nutr. 1994 Nov;72(5):775-83.
34. Lee JW, Lee KW, Lee SW, Kim IH, Rhee C. Selective increase in pinolenic acid (all-cis-5,9,12-18:3) in Korean pine nut oil by crystallization and its effect on LDL-receptor activity. Lipids. 2004 Apr;39(4):383-7.

http://www.lef.org/magazine/mag2006/jul2006_cover_calorie_01.htm

Gabriel Guzman
07-17-2006, 08:00 AM
Thanks Malcom. Although the same story has been around for some time (less calories-life extension), I'm always a bit doubtful of the actual causality of the relationship. Given what it's known about the role of telomeres in actual number of cell divisions (one could say is another, perhaps more accurate way to measure life extension and not just how many more years an organism lives), I would prefer to see results linked to that instead of just how much longer people live. I prefer to see it under a slightly different light; correcting hyperinsulinemia, which tends to correct a number of other related conditions, may not necessarily extend life but slow down the 'aging' process, which is not quite the same. One could think that in the absence of metabolic problems, we may be meant to live XX years with a 'normal' aging rate, but when hyperinsulinemia and its consequences are thrown into the equation, that aging rate may accelerate shortening lifespan. Restoring insulin homeostasis may just restore the normal aging rate, which compared to the pathological state may just seem as an extension of lifespan. I remember a similar discussion a few years ago when I posted a message on a related topic.

Another objection I always have to the less calorie story is the way calories are reduced; by suppressing appetite. More over, appetite is suppressed using this or that substance. In the end, it is total amount of food that's reduced and even though there may be reduction in fat mass, nothing is said about lean body mass and how that total food reduction affects it. If we've learned anything on PP, we've noticed that an adequate amount of protein does have an effect in appetite and people tend to reduce their food intake voluntarily (because of the increased satiety induced by more protein in the diet), while weight loss mainly from fat mass is achieved (in part by increased thermogenesis also induced by more protein in the diet). Paraphrasing the Eades, carbohydrate control and adequate protein intake may indeed be the smartest way to reducd calories. The best part is that it happens without affecting lean body weight.

The greatest obstacle faced by anyone undertaking caloric restriction and trying to achieve sustained weight reduction is the nagging sensation of feeling hungry. Most people give in to this craving and thus forgo the opportunity to reduce their risks for life-threatening diseases. Fortunately, pinolenic acid, a newly discovered phytonutrient from the Korean pine nut, increases food satisfaction and food fullness by encouraging the secretion of hormones in the gut that are intimately involved in appetite control.

This is exactly one of the most commented results from those how adhere closely to PP (can't speak for those who do something 'similar'); they don't feel hungry and that feeling of lasting satiety is what helps them in the control of food intake, which in the end results in calorie reduction but not from decreasing all incoming food, but from taking advantage of the dynamic action of the composition of their diet. At least to me, the big difference is using food as a whole instead of an isolated substance to achieve results, taking advantage of the way the body handles different nutrients without necessarily having to reduced them and, as we experience here, even increasing the amount of some of them.

mcsblues
07-17-2006, 09:16 AM
Gabe, I agree with pretty much all you say but I don't think a PP style low carb diet and any additional means of appetite suppression are necessarily mutually exclusive. I know it has become a bit of a cracked record, but I can easily overeat whilst 'adhering closely' to PP guidelines. The level of satiety is certainly better than it was when I was losing/maintaining on low fat but I put the improvement down more to stable blood sugar ahead of protein % - but I imagine both help. So I guess I will be interested to see whether this latest supplement has more going for it than a LEF sales spiel.

Oh yes, and call me a skeptic but I would still like to see a metabolic ward controlled human study showing increased fat loss through the thermogenesis of higher protein isocaloric diet! ;)

Mitra
07-17-2006, 09:34 AM
It seemed that most of the human studies mentioned were in overweight adults, and I didn't see anything to address the low bodyweight that seems likely to result if a normal weight person reduces their calories. There were references to reduced body temperature and sleeping energy expenditure, but that was only after losing quite a bit of weight.

If you are not overweight but are interested in limiting your calorie intake to promote longevity and reduce disease risk, pinolenic acid can help enhance satiety and control appetite, critical factors involved in decreasing calorie intake.

It didn't mention how you were supposed to do this without becoming underweight. While I can easily eat more than I do (and gain weight), I don't find it particularly difficult to eat less - but when that happens, I lose weight, and Shadow tells me off ;). I know that most of the studies that say what weight is healthy are epidemiological, so the underweight people might well be suffering from some illness, or be getting less than adequate nutrition, and may not be representative of people who make every effort to eat nutritionally dense food, but I'd still want to see a bit more information in this area before deliberately heading that way!

Gabriel Guzman
07-17-2006, 10:35 AM
Oh yes, and call me a skeptic but I would still like to see a metabolic ward controlled human study showing increased fat loss through the thermogenesis of higher protein isocaloric diet! ;)

And you may never see it because such change is unlikely to happen during a very short-period of time. Increased thermogenesis has been shown several times. But the actual measurement of the impact in fat loss needs a longer time than any metabolic ward study can go, mainly because of the cost of a, say 4-month study. Besides, you would have to add the cost of a psychologist after the subjects get out of there!!!

I'm always amazed that some people like to think of metabolic changes as something that happens overnight, completely discounting the adaptation that has to occur before any changes take place. As I wrote before, thermogenesis is part of the mechanisms, not the only one taking place in diets similar to PP in terms of the amount of protein. And even if the contribution is to some very little, that very little over a long period of time makes a lot of difference

Anyway, I suppose is a matter of personal choice to rely on supplements to achieve one's goals at a certain time (most likely 'now'!) or to take advantage of the effects of food itself, which is just as effective but it takes a little longer.

laughingW
07-17-2006, 11:05 AM
I wonder why they tried that isolated substance in the first place.

Seems to me I get the exact same effect using macadamia nuts as between meal snacks - extremely satisfied and when I run my calorie numbers in Fitday, they are sometimes low by govt standards, but when I look at my nutrient report, all the nutrients are there. Well as many as Fitday shows.

LisaS
07-17-2006, 01:25 PM
It didn't mention how you were supposed to do this without becoming underweight. While I can easily eat more than I do (and gain weight), I don't find it particularly difficult to eat less - but when that happens, I lose weight


they kind of hinted at a mechanism when they mentioned body temp - it seems like this is aimed at lowering your BMR - and lower BMR will let you maintain weight at lower calorie levels -

from the article: Core body temperature also fell in the calorie-restriction and calorie-restriction-with-exercise groups. Absolute 24-hour energy expenditure and sleeping energy expenditure decreased in all treatment groups, and the effect was more than could be explained by changes in body composition (fat loss). The researchers concluded that caloric restriction induced a “metabolic adaptation”—that is, a reduction in the baseline rate at which the body burns fuel. This adaptation is desirable for the purpose of slowing aging. People seeking to improve fitness and lose weight often exercise vigorously in the hope that exercise will boost their metabolic rate.

it seems like they do this intentionally for a longevity effect whereas dieters try to avoid this like the plague to prevent stalling :D

Mitra
07-17-2006, 02:14 PM
But the paragraph before that said:
On average, body weight decreased by 10% in the calorie-restriction and calorie-restriction-with-exercise groups, while body fat decreased by 24-25%. The subjects on a very low-calorie diet lost 13.9% of their initial body weight and 32% of their body fat. By contrast, body weight remained virtually unchanged in the control subjects.

So it doesn't seem as if this would be a good thing to do unless you had the spare capacity to accommodate a degree of loss while you wait for your body to do all this adjusting. But then, if you did have the weight to lose, you wouldn't want your body to adjust, because then it would be harder to lose the rest of your excess. Sounds like you're stuck either way ;).

mcsblues
07-17-2006, 09:15 PM
And you may never see it because such change is unlikely to happen during a very short-period of time. Increased thermogenesis has been shown several times. But the actual measurement of the impact in fat loss needs a longer time than any metabolic ward study can go, mainly because of the cost of a, say 4-month study. Besides, you would have to add the cost of a psychologist after the subjects get out of there!!!

I'm always amazed that some people like to think of metabolic changes as something that happens overnight, completely discounting the adaptation that has to occur before any changes take place. As I wrote before, thermogenesis is part of the mechanisms, not the only one taking place in diets similar to PP in terms of the amount of protein. And even if the contribution is to some very little, that very little over a long period of time makes a lot of difference
I'm interested in what part of protein metabolism requires adaptation before it becomes thermogenic. I would have thought it either is or it isn't. If one needs to adapt to a higher % of protein for this effect to be noticeable, are you saying that adaptation makes the utilization of protein less efficient either as an energy source or for the body to metabolise it for other purposes as time goes by? If there is such a difference after adaptation then it should be apparent by comparing subjects before and after adoption of a high protein diet - they surely wouldn't need to stay locked away for the intervening weeks or months?

Anyway, I suppose is a matter of personal choice to rely on supplements to achieve one's goals at a certain time (most likely 'now'!) or to take advantage of the effects of food itself, which is just as effective but it takes a little longer.
You are assuming that supplementation is being used for quick weight loss, wheras as I see it, such a supplement (or perhaps the pine nuts or whatever) would be just as useful (probably more) for maintenance. I'm sure the majority of us continue to take quite a few of the supplements that the Eades recommend for health reasons alone and a natural appetite suppressant would be a useful addition in my view ... if it works!

I don't know, maybe I am the exception ... or just exceptionally greedy/food addicted! Laughing W, I would love for maccadamias to work in the way you describe, but for me they are a very occasional almost guilty pleasure that I only buy 100g at a time ... as I know they won't make it home from the supermarket!!

As for the calorie restriction thing generally, I agree that some skepticism is required when looking at studies involving mice and flies! But if insulin is an aging hormone, then perhaps it is beneficial to restrict protein intake (and with it calories) to close to the PP minimums, rather than to be too liberal with the 'if still hungry eat low carb snacks' idea, as even if balanced with glucagon, more insulin than necessary will be produced as a result.

Gabriel Guzman
07-17-2006, 11:09 PM
Nope, all I'm saying is that there is a tendency to look at the immediate results of, say increasing protein intake and although thermogenesis is measureable and indicates increase in metabolic rate, the actual substantial fat loss due to that may not be observed just as quickly. Adaptation doesn't make use of protein less efficient (don't know where you got the idea...), it actually means the time it takes the body to start making enzymes that were not made before. The last thing the body would do is to use protein as an energy source, hence the sparing effect of ketone utilization and that also comes after a period of adaptation resulting not in less but more efficiency in using the new substrate.

We're not talking about losing a couple of pounds due to increase thermogenesis. You said you'd like to see experiments done in metabolic wards where fat loss can be shown due to increase thermogenesis so I suggested that to put fat loss entirely on thermogenesis, or to actually achieve fat loss only through thermogenesis, the study would have to be not a short one and is unlikely that you can have people locked in for that long. I also said that thermogenesis is just one of the adaptations to more protein in the diet and that plays a role. So, again, you're taking individual factors that may not act individually in something as complex but that sounds as simple as 'weight loss'.

To me it makes no sense at all to restrict an absolutely required nutrient that has very little to do with hyperinsulinemia in order to achieve caloric restriction or life extension. Protein intake doesn't cause hyperinsulinemia. In fact, it has been shown that a change in the ratio carbohyrate-to-protein (in favor of more protein) actually results in better postprandial insulin response and better normoglycemia.

Now to think that weight loss supplements are not used to achieve some kind of accelerated effect may be a bit naive. Being because they block the absorption of an important nutrient, or because they decrease apetite, their market wouldn't be as lucrative as it is if people wouldn't think would help them slim fast (no pun intended).

Incidentally, since you mentioned flies, a few years back somebody showed that by not letting flies have their progeny he could extend their lifes up to 20-somthing times their normal lifespan. In esence, they removed the eggs after the flies laid them and the flies literally refused to die until they laid another batch of eggs. They played the same trick over and over and the flies just wouldn't die... When they decided to leave the eggs, the adult flies started to die as they would normally do. Calories had nothing to do with the experiment and the hypothesis is that the pressure of producing offspring in order to preserve the species is what drove their 'refusal to die'. True or not it's interesting... calories aside. I don't even want to speculate how would that apply to humans, but that's just another story that has to do with lifespan extension.

mcsblues
07-18-2006, 01:01 AM
I think any discussion we have here should be seen in the light of who we are (committed low carbers) - sure some (other) people might leap at any new supplement or food which will help the latest crash diet fad. I'm not sure that I care about them!

'We' OTOH eat a higher protein percentage than the SAD - for a lot of reasons, but one of them is appetite suppression through the satiety of protein itself - so I don't think adding something like pine nuts to our diet for similar reasons should be seen as an aberration, just like coconut oil has been used by some here for more than just it's quality fats.

The only reason I raised the strange possibility of increasing inefficiency is the timescale you suggested would be needed to see significant results. If adaptation means increasing efficiency (as you would expect) then the so called metabolic advantage (be that a combination of factors) should be at it's most pronounced in the first few weeks of any study and easily discernable.

On the calorie restriction front (a) it is entirely academic because I can't see myself doing it!:) and (b) I'm not suggesting protein restriction to an extent where intake is insufficient for muscle building/maintenance but rather a maximum figure might be set rather than the free rein the Eades give you above the minimum values they suggest. In other words the macronutrient ratios would remain the same but less total calories consumed.

In that scenario, wouldn't less insulin be produced? Is it possible that a further slowing of the aging process would result? Sure we aren't talking about hyperinsulinemia any more but there are said to be substantial benefits from keeping blood sugar well below the prediabetic range (I forget the study but it showed a significant increase in risk as fasting levels rose from 80 to 90) - one would imagine insulin is no different - in fact it may well be the main cause of the problems associated with those blood sugar findings.

mcsblues
07-18-2006, 10:39 AM
Just to confuse the issue further, this (http://www.nutritionandmetabolism.com/content/pdf/1743-7075-3-25.pdf) new paper looks at 'adaptive thermogenesis' as a potential result of overfeeding, and at least in that context they are clearly using that phrase to indicate possible increased inefficiency not explained by additional energy expenditure required to gain weight or the energy costs of maintaining a higher body weight.

It is way past my bed time - so I have only skipped through it, but the picture is probably confused somewhat by the comparison of studies done with large variations in macronutrient intake.

I look forward to your translation in the morning!:)

Billie
07-19-2006, 07:08 AM
Malcom since we discussed it over dinner, and you know he definitely has an opinion ;) I am sure he will respond. I kept him away from the computer last night!:evil: