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High Milk Protein Lowers Stress

“One of the reasons a lot of people give, if they have overcome the idea that milk forms mucous, or is a risk for diseases and so on; one of their arguments is that it makes them fat. But, all the research on animals, and as far as it goes, human research, shows that milk is probably the best reducing foods there is. The mechanisms for that are now known. Not only the anti-stress effects of casein, and a good balance of saturated fats and so on, but the calcium alone is very important metabolic regulator, that it happens to inhibit the fat-forming enzymes fatty acid synthase, and incidentally that’s a characteristic enzyme that goes wild in cancer. But calcium and milk inhibit that fatty acid synthase, reducing the formation of fats and at the same time it activates the uncoupling proteins in the mitochondria, which are associated with increased longevity. Because they, by increasing the metabolic rate, the uncoupling proteins burn calories faster but they protect against free-radical oxidation. That they pull the fuel through the oxidation process so fast in effect, that none of it goes astray in random oxidation, where if you inhibit your energy producing enzymes you tend to get random, stray oxidation that damage the mitochondria. So the uncoupling proteins burn calories faster, at the same time that your reducing fat synthesis and milk is, as far as I know, they only food does both of those things simultaneously.” -Ray Peat, PhD

Indian J Exp Biol. 2003 Apr;41(4):367-9.
Protection of adrenocortical activity by dietary casein in ether anaesthetized rats.
Biswas NM, Chattopadhyay A, Sarkar M.
Adrenal delta5-3beta-hydroxysteroid dehydrogenase (delta5-3beta-HSD) activity and serum corticosterone level were significantly higher in rats fed with 5% casein or 4% albumin diets after 1 hr of ether anaesthetic stress as compared to the controls, 5% casein and 20% casein (equivalent to 4% albumin) respectively. Ether anaesthesia to 20% casein fed rats caused no change in adrenal delta5-3beta-HSD activity and serum corticosterone level when compared with controls fed 20% casein diet. The results suggest that high milk protein diet may prevent acute stress effects by protecting adrenocortical activity. The present investigation opens up a new area of management of stress.

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By Team FPS – June 3, 2012

Autoimmunity, Thyroiditis, and Intestinal Flora

Also see:
Ray Peat, PhD on the Benefits of the Raw Carrot
How does estrogen enhance endotoxin toxicity? Let me count the ways.
Autoimmune Disease and Estrogen Connection
The effect of raw carrot on serum lipids and colon function
Protective Bamboo Shoots
Endotoxin: Poisoning from the Inside Out
Hypothyroidism, Intestinal Bacterial Overgrowth, & Lactose Intolerance

“Endotoxin or other materials absorbed from intestinal bacteria contributes to a variety of autoimmune problems, including thyroiditis (Penhale and Young, 1988). Combining indigestible fiber, such as raw carrot, with mild germicides, such as vinegar and coconut oil, can improve the hormonal environment, while reducing the immunological burden.” -Ray Peat, PhD from “Thyroiditis. Some confusions and causes of “autoimmune disease””

Clin Exp Immunol. 1988 May;72(2):288-92.
The influence of the normal microbial flora on the susceptibility of rats to experimental autoimmune thyroiditis.
Penhale WJ, Young PR.
Female PVG/c strain rats maintained under specific pathogen-free conditions until weaning were found to be significantly less susceptible to the induction of autoimmune thyroiditis by thymectomy and irradiation than conventionally reared rats of the same strain. Other SPF-derived strains had a similarly low susceptibility, thus pointing to an important external factor influencing the induction of autoimmunity by this procedure. It was found that the oral administration of antibiotics followed by fresh, homogenized, intestinal contents obtained from conventionally reared rats to newly weaned SPF PVG/c rats significantly augmented their autoimmune susceptibility. The offspring of female SPF rats which had been treated in late pregnancy with oral antibiotics and conventional intestinal contents were similarly more susceptible than the offspring of non-treated counterparts. It is proposed that the composition of the normal gastrointestinal flora of conventionally reared rats profoundly influences susceptibility to the induction of autoimmune thyroiditis in this particular experimental model, possibly by antigenic cross-reactivity with thyroid tissue.

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By Team FPS – June 2, 2012

Ovarian Cysts

Also see:
Estrogen, Uterine Fibroids, and Thyroid Nodules
Quotes: Thyroid, Estrogen, Menstrual Symptoms, PMS, and Infertility
Autoimmune Disease and Estrogen Connection
Hormonal profiles in women with breast cancer
PUFA Increases Estrogen
PUFA Inhibit Glucuronidation
PUFA Promote Cancer
Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring
Vitamin A: Anti-Cancer and Anti-Estrogen
Toxic Plant Estrogens
The Dire Effects of Estrogen Pollution
Progesterone: Essential to Your Well-Being
Alcohol Consumption – Estrogen and Progesterone In Women
Estrogen, Endotoxin, and Alcohol-Induced Liver Injury
Estrogen Levels Increase with Age
Fat Tissue and Aging – Increased Estrogen
Estrogen Related to Loss of Fat Free Mass with Aging
Bisphenol A (BPA), Estrogen, and Diabetes
Shock Increases Estrogen

“Animal experiments show that lack of thyroid hormone can cause cystic ovaries.” -Ray Peat, PhD in “Nutrition for Women”

“Animals which are artificially made hypothyroid develop cystic ovaries, so it is reasonable to consider hypothyroidism as an important factor when women have cystic ovaries.” -Ray Peat, PhD

“In my own experience, no patient has required a hysterectomy for pathological bleeding unless uterine fibroids were present. If organic problems could be ruled out, as they could in the great majority of cases, thyroid deficiency usually could be detected and treatment with thyroid solved the problem. The need for other surgery may be minimized by adequate thyroid therapy in women with low thyroid function. Cysts on the ovary are common in such women and correction of the thyroid deficiency often eliminates the cysts. Fibroid tumors have been rare in hypothyroid women who have been maintained on adequate thyroid therapy. It is possible to produce fibroids in experimental animals by injection of estrogen, and there is evidence of excess of estrogen in hypothyroid women.” -Dr. Broda Barnes

Animal Reproduction Science Volume 39, Issue 2 , Pages 159-168, July 1995
The importance of thyroid hormone in experimental ovarian cyst formation in gilts
Remigiusz Fitko, Jan Kucharski, Beata Szlezyngier

The Anatomical Record Volume 90, Issue 2, pages 93–99, October 1944
Occurrence of follicular cysts in thyroidectomized rats treated with diethylstilbestrol
Ralph G. Janes

The Anatomical Record Volume 131, Issue 3, pages 487–499, July 1958
Hormonal influences on the gonadotrophin sensitive hypothyroid rat ovary
James H. Leathem

Proc Soc Exp Biol Med. 1991 Nov;198(2):737-41.
Circulating hormone concentrations in hypothyroid rats with induced polycystic ovaries.
Lee MT, Adams WC, Bruot BC.

Biol Reprod. 1986 Oct;35(3):542-8.
Hormonal changes during the early development of ovarian cysts in the rat.
Lee MT, Bruot BC, Adams WC.

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By Team FPS – May 31, 2012

Preventing Breast Cancer

Preventing Breast Cancer by John Gofman, MD

Alice Stewart: The woman who knew too much
Alice Mary Stewart
Alice Stewart, 95; Linked X-Rays to Diseases
Dr. Alice Stewart, Low-Level Radiation, and the Fetus
Book: The Woman Who Knew Too Much: Alice Stewart and the Secrets of Radiation
Inflammation from Radiation
Harm of Prenatal Exposure to Radiation
Caffeine and Skin Protection
Topical Vitamin E and ultraviolet radiation on human skin
Radiation and Growth – Ray Peat
Bone Density: First Do No Harm
Executive Summary, Radiation from Medical Procedures in the Pathogenesis of Cancer and Ischemic Heart Disease: Dose-Response Studies with Physicians per 100,000 Population
Quotes and more from Dr. John Gofman
John W. Gofman, 88, Scientist and Advocate for Nuclear Safety, Dies
Breast Cancer

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By Team FPS – May 29, 2012

Ben Goldacre: Battling bad science

Also see:
What Doctors Don’t Know About the Drugs They Prescribe

So I’m a doctor, but I kind of slipped sideways into research, and now I’m an epidemiologist. And nobody really knows what epidemiology is. Epidemiology is the science of how we know in the real world if something is good for you or bad for you. And it’s best understood through example as the science of those crazy, wacky newspaper headlines. And these are just some of the examples.

These are from the Daily Mail. Every country in the world has a newspaper like this. It has this bizarre, ongoing philosophical project of dividing all the inanimate objects in the world into the ones that either cause or prevent cancer. So here are some of the things they said cause cancer recently: divorce, Wi-Fi, toiletries and coffee. Here are some of the things they say prevents cancer: crusts, red pepper, licorice and coffee. So already you can see there are contradictions. Coffee both causes and prevents cancer. And as you start to read on, you can see that maybe there’s some kind of political valence behind some of this. So for women, housework prevents breast cancer, but for men, shopping could make you impotent. So we know that we need to start unpicking the science behind this.

And what I hope to show is that unpicking dodgy claims, unpicking the evidence behind dodgy claims, isn’t a kind of nasty carping activity; it’s socially useful, but it’s also an extremely valuable explanatory tool. Because real science is all about critically appraising the evidence for somebody else’s position. That’s what happens in academic journals. That’s what happens at academic conferences. The Q&A session after a post-op presents data is often a blood bath. And nobody minds that. We actively welcome it. It’s like a consenting intellectual S&M activity. So what I’m going to show you is all of the main things, all of the main features of my discipline — evidence-based medicine. And I will talk you through all of these and demonstrate how they work, exclusively using examples of people getting stuff wrong.

So we’ll start with the absolute weakest form of evidence known to man, and that is authority. In science, we don’t care how many letters you have after your name. In science, we want to know what your reasons are for believing something. How do you know that something is good for us or bad for us? But we’re also unimpressed by authority, because it’s so easy to contrive. This is somebody called Dr. Gillian McKeith Ph.D, or, to give her full medical title, Gillian McKeith. (Laughter) Again, every country has somebody like this. She is our TV diet guru. She has massive five series of prime-time television, giving out very lavish and exotic health advice. She, it turns out, has a non-accredited correspondence course Ph.D. from somewhere in America. She also boasts that she’s a certified professional member of the American Association of Nutritional Consultants, which sounds very glamorous and exciting. You get a certificate and everything. This one belongs to my dead cat Hetti. She was a horrible cat. You just go to the website, fill out the form, give them $60, and it arrives in the post. Now that’s not the only reason that we think this person is an idiot. She also goes and says things like, you should eat lots of dark green leaves, because they contain lots of chlorophyll, and that will really oxygenate your blood. And anybody who’s done school biology remembers that chlorophyll and chloroplasts only make oxygen in sunlight, and it’s quite dark in your bowels after you’ve eaten spinach.

Next, we need proper science, proper evidence. So, “Red wine can help prevent breast cancer.” This is a headline from the Daily Telegraph in the U.K. “A glass of red wine a day could help prevent breast cancer.” So you go and find this paper, and what you find is it is a real piece of science. It is a description of the changes in one enzyme when you drip a chemical extracted from some red grape skin onto some cancer cells in a dish on a bench in a laboratory somewhere. And that’s a really useful thing to describe in a scientific paper, but on the question of your own personal risk of getting breast cancer if you drink red wine, it tells you absolutely bugger all. Actually, it turns out that your risk of breast cancer actually increases slightly with every amount of alcohol that you drink. So what we want is studies in real human people.

And here’s another example. This is from Britain’s leading diet and nutritionist in the Daily Mirror, which is our second biggest selling newspaper. “An Australian study in 2001 found that olive oil in combination with fruits, vegetables and pulses offers measurable protection against skin wrinklings.” And then they give you advice: “If you eat olive oil and vegetables, you’ll have fewer skin wrinkles.” And they very helpfully tell you how to go and find the paper. So you go and find the paper, and what you find is an observational study. Obviously nobody has been able to go back to 1930, get all the people born in one maternity unit, and half of them eat lots of fruit and veg and olive oil, and then half of them eat McDonald’s, and then we see how many wrinkles you’ve got later.

You have to take a snapshot of how people are now. And what you find is, of course, people who eat veg and olive oil have fewer skin wrinkles. But that’s because people who eat fruit and veg and olive oil, they’re freaks, they’re not normal, they’re like you; they come to events like this. They are posh, they’re wealthy, they’re less likely to have outdoor jobs, they’re less likely to do manual labor, they have better social support, they’re less likely to smoke — so for a whole host of fascinating, interlocking social, political and cultural reasons, they are less likely to have skin wrinkles. That doesn’t mean that it’s the vegetables or the olive oil.

(Laughter)

So ideally what you want to do is a trial. And everybody thinks they’re very familiar with the idea of a trial. Trials are very old. The first trial was in the Bible — Daniel 1:12. It’s very straightforward — you take a bunch of people, you split them in half, you treat one group one way, you treat the other group the other way, and a little while later, you follow them up and see what happened to each of them. So I’m going to tell you about one trial, which is probably the most well-reported trial in the U.K. news media over the past decade. And this is the trial of fish oil pills. And the claim was fish oil pills improve school performance and behavior in mainstream children. And they said, “We’ve done a trial. All the previous trials were positive, and we know this one’s gonna be too.” That should always ring alarm bells. Because if you already know the answer to your trial, you shouldn’t be doing one. Either you’ve rigged it by design, or you’ve got enough data so there’s no need to randomize people anymore.

So this is what they were going to do in their trial. They were taking 3,000 children, they were going to give them all these huge fish oil pills, six of them a day, and then a year later, they were going to measure their school exam performance and compare their school exam performance against what they predicted their exam performance would have been if they hadn’t had the pills. Now can anybody spot a flaw in this design? And no professors of clinical trial methodology are allowed to answer this question. So there’s no control; there’s no control group. But that sounds really techie. That’s a technical term. The kids got the pills, and then their performance improved.

What else could it possibly be if it wasn’t the pills? They got older. We all develop over time. And of course, also there’s the placebo effect. The placebo effect is one of the most fascinating things in the whole of medicine. It’s not just about taking a pill, and your performance and your pain getting better. It’s about our beliefs and expectations. It’s about the cultural meaning of a treatment. And this has been demonstrated in a whole raft of fascinating studies comparing one kind of placebo against another. So we know, for example, that two sugar pills a day are a more effective treatment for getting rid of gastric ulcers than one sugar pill. Two sugar pills a day beats one sugar pill a day. And that’s an outrageous and ridiculous finding, but it’s true. We know from three different studies on three different types of pain that a saltwater injection is a more effective treatment for pain than taking a sugar pill, taking a dummy pill that has no medicine in it — not because the injection or the pills do anything physically to the body, but because an injection feels like a much more dramatic intervention. So we know that our beliefs and expectations can be manipulated, which is why we do trials where we control against a placebo — where one half of the people get the real treatment and the other half get placebo.

But that’s not enough. What I’ve just shown you are examples of the very simple and straightforward ways that journalists and food supplement pill peddlers and naturopaths can distort evidence for their own purposes. What I find really fascinating is that the pharmaceutical industry uses exactly the same kinds of tricks and devices, but slightly more sophisticated versions of them, in order to distort the evidence that they give to doctors and patients, and which we use to make vitally important decisions.

So firstly, trials against placebo: everybody thinks they know that a trial should be a comparison of your new drug against placebo. But actually in a lot of situations that’s wrong. Because often we already have a very good treatment that is currently available, so we don’t want to know that your alternative new treatment is better than nothing. We want to know that it’s better than the best currently available treatment that we have. And yet, repeatedly, you consistently see people doing trials still against placebo. And you can get license to bring your drug to market with only data showing that it’s better than nothing, which is useless for a doctor like me trying to make a decision.

But that’s not the only way you can rig your data. You can also rig your data by making the thing you compare your new drug against really rubbish. You can give the competing drug in too low a dose, so that people aren’t properly treated. You can give the competing drug in too high a dose, so that people get side effects. And this is exactly what happened which antipsychotic medication for schizophrenia. 20 years ago, a new generation of antipsychotic drugs were brought in and the promise was that they would have fewer side effects. So people set about doing trials of these new drugs against the old drugs, but they gave the old drugs in ridiculously high doses — 20 milligrams a day of haloperidol. And it’s a foregone conclusion, if you give a drug at that high a dose, that it will have more side effects and that your new drug will look better.

10 years ago, history repeated itself, interestingly, when risperidone, which was the first of the new-generation antipscyhotic drugs, came off copyright, so anybody could make copies. Everybody wanted to show that their drug was better than risperidone, so you see a bunch of trials comparing new antipsychotic drugs against risperidone at eight milligrams a day. Again, not an insane dose, not an illegal dose, but very much at the high end of normal. And so you’re bound to make your new drug look better. And so it’s no surprise that overall, industry-funded trials are four times more likely to give a positive result than independently sponsored trials.

But — and it’s a big but — (Laughter) it turns out, when you look at the methods used by industry-funded trials, that they’re actually better than independently sponsored trials. And yet, they always manage to to get the result that they want. So how does this work? How can we explain this strange phenomenon? Well it turns out that what happens is the negative data goes missing in action; it’s withheld from doctors and patients. And this is the most important aspect of the whole story. It’s at the top of the pyramid of evidence. We need to have all of the data on a particular treatment to know whether or not it really is effective. And there are two different ways that you can spot whether some data has gone missing in action. You can use statistics, or you can use stories. I personally prefer statistics, so that’s what I’m going to do first.

This is something called funnel plot. And a funnel plot is a very clever way of spotting if small negative trials have disappeared, have gone missing in action. So this is a graph of all of the trials that have been done on a particular treatment. And as you go up towards the top of the graph, what you see is each dot is a trial. And as you go up, those are the bigger trials, so they’ve got less error in them. So they’re less likely to be randomly false positives, randomly false negatives. So they all cluster together. The big trials are closer to the true answer. Then as you go further down at the bottom, what you can see is, over on this side, the spurious false negatives, and over on this side, the spurious false positives. If there is publication bias, if small negative trials have gone missing in action, you can see it on one of these graphs. So you can see here that the small negative trials that should be on the bottom left have disappeared. This is a graph demonstrating the presence of publication bias in studies of publication bias. And I think that’s the funniest epidemiology joke that you will ever hear.

That’s how you can prove it statistically, but what about stories? Well they’re heinous, they really are. This is a drug called reboxetine. This is a drug that I myself have prescribed to patients. And I’m a very nerdy doctor. I hope I try to go out of my way to try and read and understand all the literature. I read the trials on this. They were all positive. They were all well-conducted. I found no flaw. Unfortunately, it turned out, that many of these trials were withheld. In fact, 76 percent of all of the trials that were done on this drug were withheld from doctors and patients. Now if you think about it, if I tossed a coin a hundred times, and I’m allowed to withhold from you the answers half the times, then I can convince you that I have a coin with two heads. If we remove half of the data, we can never know what the true effect size of these medicines is.

And this is not an isolated story. Around half of all of the trial data on antidepressants has been withheld, but it goes way beyond that. The Nordic Cochrane Group were trying to get a hold of the data on that to bring it all together. The Cochrane Groups are an international nonprofit collaboration that produce systematic reviews of all of the data that has ever been shown. And they need to have access to all of the trial data. But the companies withheld that data from them, and so did the European Medicines Agency for three years.

This is a problem that is currently lacking a solution. And to show how big it goes, this is a drug called Tamiflu, which governments around the world have spent billions and billions of dollars on. And they spend that money on the promise that this is a drug which will reduce the rate of complications with flu. We already have the data showing that it reduces the duration of your flu by a few hours. But I don’t really care about that. Governments don’t care about that. I’m very sorry if you have the flu, I know it’s horrible, but we’re not going to spend billions of dollars trying to reduce the duration of your flu symptoms by half a day. We prescribe these drugs, we stockpile them for emergencies on the understanding that they will reduce the number of complications, which means pneumonia and which means death. The infectious diseases Cochrane Group, which are based in Italy, has been trying to get the full data in a usable form out of the drug companies so that they can make a full decision about whether this drug is effective or not, and they’ve not been able to get that information. This is undoubtedly the single biggest ethical problem facing medicine today. We cannot make decisions in the absence of all of the information.

So it’s a little bit difficult from there to spin in some kind of positive conclusion. But I would say this: I think that sunlight is the best disinfectant. All of these things are happening in plain sight, and they’re all protected by a force field of tediousness. And I think, with all of the problems in science, one of the best things that we can do is to lift up the lid, finger around in the mechanics and peer in.

Thank you very much.

(Applause)

Source


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By Team FPS – May 6, 2012

180 Program Testimonial – Protective Nutrition

Male, 38, Canada

1. What was the primary benefit of doing the Program for you?

For me, it was mostly about learning and putting together in a more organized fashion, all of the elements that form a protective nutritional approach based on Peat’s ideas.

2. Did you experience changes in energy, appetite, emotional balance, and mental sharpness?

Those were not issues for me…I went from intermittent fasting to using a more regular eating pattern but, overall, this did little for me in terms of energy, appetite, emotional balance and mental sharpness.

3. How long did you spend in calendar time on the Program?

The whole 16 weeks, and still going, with no plans to revert back to any other type of nutritional approach.

4. What were your body temperature and pulse changes during the Program?

Significant. Pulse went up a bit but, temperature, on average (armpit), went up more than 2 degrees!

5. Would you recommend the Program to others?

YES.

6. Was the information presented understandable and credible?

Thoroughly, yes.

7. Was your coach for the Program helpful? What grade would you give him/her? (A – F)

Very helpful. Very approachable. And always backing up his sources and giving great advice with regards to supplementation and other concerns.

8. Is it easy to procure the foods you need and prepare them for the Program you are now using?

Yes.

9. Did you have identified problems upon entering the Program, and were they changed?

Yes. Minor skin issues have all but disappeared. Same with canker sores. I know what I’ve done wrong now when I do get them (usually, too much starch).

10. Summarize your experience with the program.

This was a very worthwhile experience for me and, I am confident it has allowed me to gain a better grasp of the sometimes abstract notions presented by Peat. I am also quite confident it will allow me to use the acquired knowledge for easing further learning experiences as I continue to delve into Peat’s writings, as well as for using the principles with family members, clients and the likes.

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By Team FPS – May 4, 2012

180 Program Testimonial – Follow Up – Smarter Not Harder

Female, age 32, VA & CA

How has the continued use of the 180 Program nutrition principles helped you?

It’s been 18 months since I started the 180 program. The following are benefits that I’ve experienced since beginning and maintaining this way of life:

  • Weight loss (formerly a size 8, I am now a size 2-4). I’ve lost 20+ pounds and it continues to come off. My body is still changing for the better as I continue the program.
  • Loss of bloating and puffiness in body and face
  • No PMS, regular cycles, no cramping, no mood swings
  • 100% improvement in all digestive issues and regularity
  • Better, more restful sleep (I’ve made it a priority in my life to get to bed early, especially during the week. This also includes no tv before bed or falling asleep with the tv on. It makes a huge difference).
  • Clear, glowing skin (I only use coconut oil on my face and body now as a moisturizer instead of expensive products that I used to purchase at salons that contained chemicals. I formerly had issues with breakouts and sensitivity to any skin products. Coconut oil is a natural moisturizer that works better than any product on the market and it’s inexpensive. I highly recommend this – especially for women).
  • 100% improvement in mood and happiness and no anxiety
  • Off all medications from dermatologist for skin issues
  • Off all medication for anxiety and depression from my doctor (formerly prescribed Lexapro and Diazepam)
  • Off all “vitamins/supplements” that I thought I needed
  • Improved libido
  • Increased exposure to light and sunshine (I’ve made it a priority in my life to spend as much time as possible being outdoors, soaking in the sunshine. I’ve found that is has improved my general mood, makes me happier, helps me to sleep better and look better). Light matters. Your body needs it.

What have you gained from the less is more philosophy as it applies to exercise?

I’m a lifelong athlete and former workout fanatic with a very competitive personality. I was obsessive about it. 6 days a week, 2 hours a day – that was me in the gym. I used to be so stressed out about when I could get there – my entire life revolved around it. Whether I had to wake up at 4 or 5am to fit it in or 10pm at night – I always HAD TO get there. I put so much pressure on myself and no matter what I did, I only saw minimal results. Over the years I’ve spent thousands of dollars on personal trainers and had no free time to enjoy anything else in life. I was beating up my body and had nothing to show for it except lost money, pain and inflammation.

I committed to changing my ways when I started this program (even though I fought it like crazy in the beginning). I wanted to see if there was anything else that could work. I still go to the gym once in a while now, and when I do, it’s for a maximum of 30 minutes. No more personal trainers screaming at me to do more, more, more. Now I do a little bit of cardio or weights, stretching or yoga. I’m in and out. A couple times a week, max. I’d much rather spend my time outside walking or relaxing in the sunshine.

All I had to do was stop putting stress on my body and commit to following the food portion of the program and I continue to shrink. Over-exercising DOES NOT work. As I mentioned, since I’ve changed my ways with exercising, I’ve gone from a size 8 to a size 2-4. I’ve lost over 20 pounds. My size 4 skinny jeans are falling off. Even my feet got smaller.

I have extra time in my life now to do things that make me happy. One of them includes shopping for smaller clothes. On top of everything else, I’m saving a ton of money, I’m thrilled with the way I look and my body is calm and at peace and so is my mind. It’s the exact opposite of anything I’ve ever been taught but it works and I’m a better person because of it.

If you have the discipline and make the time to give this program your 100% attention, you will be successful. It’s not magic – it takes work, but if I can do it, anyone can.

 

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By Team FPS – May 2, 2012

Statins Activate the Formation of AA from LA

Also see –
Arachidonic Acid’s Role in Stress and Shock
Anti-Inflammatory Omega -9 Mead Acid (Eicosatrienoic acid)

In adults, prostaglandins are known to be involved in many of the harmful effects of inflammation. They are formed from the polyunsaturated fats, linoleic acid and arachidonic acid, which we are unable to synthesize ourselves, so the adult’s exposure to the prostaglandins is influenced by diet. -Ray Peat, PhD

Prostaglandins Leukot Essent Fatty Acids. 2002 Aug-Sep;67(2-3):85-9.
Regulation of PUFA metabolism: pharmacological and toxicological aspects.
Risé P, Marangoni F, Galli C.
Levels of the long-chain polyunsaturated fatty acids (LCP) of the n-6 and n-3 series in animal plasma and cells are directly or indirectly dependent upon the intakes of either their precursors, the short-chain polyunsaturated fatty acids (SCP), linoleic (LA, 18:2 n-6) and alpha linolenic acid (ALA, 18:3 n-3), respectively, and/or of the preformed products (arachidonic, 20:4 n-6) and eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3). We report here that pharmacological agents and cytotoxic compounds significantly affect the production of LCP from SCP in cultured cells. Using labelled substrates and radio HPLC separations, we observed that the potent hypocholesterolemic agent, simvastatin, activates the formation of AA from LA, mainly acting at the delta5 desaturation step, and increases also the mRNA levels, in cultured monocytic cells (THP-1). Elevation of AA occurs also in plasma lipids of hyperlipemic patients treated with statins (but not with fibrates). Conversely, oxysterols (mainly 7-beta-oxysterol), which are detected in circulating lipoproteins of rabbits on a hypercholesterolemic diet, potently inhibit the synthesis of AA from LA in hepatocytic cell lines (Hep-G2). At the same time plasma levels of AA are reduced vs controls, in spite of an identical intake of LA. Finally, on the basis of previous work showing reduced levels of LCP, mainly DHA, in the milk of cigarette-smoking mothers, we have observed that the incubation of human mammary gland cells with sera exposed to cigarette smoke results in marked inhibition of the production of DHA from ALA. The products in smoke responsible for this effect, are being identified through mass spectrometric techniques. In conclusion, pharmacological agents and toxic compounds, such as oxysterols and smoke products affect key steps in the synthesis of the LCP, major bioregulators in mammalian cells.

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By Team FPS – April 29, 2012

TV Watching, Body Fatness, and Diet in Preschool Children

Am J Clin Nutr. 2009 Apr;89(4):1031-6. Epub 2009 Feb 25.
Increased television viewing is associated with elevated body fatness but not with lower total energy expenditure in children.
Jackson DM, Djafarian K, Stewart J, Speakman JR.
BACKGROUND:
Television (TV) viewing in children is associated with a higher body mass index, but it is unknown whether this reflects body fatness, and, if it does, why.
OBJECTIVE:
The objective was to investigate whether TV viewing is associated with body fatness, physical activity, and total energy expenditure in preschool children.
DESIGN:
Eighty-nine children were recruited into a cross-sectional study. Total daily energy expenditure (TEE) was measured by doubly labeled water, body composition by dual-energy X-ray absorptiometry, and physical activity by accelerometry.
RESULTS:
There was a significant positive association between fat mass (corrected for fat-free body mass) and TV viewing (F = 9.05, P = 0.004). Each extra hour of watching TV was associated with an extra 1 kg of body fat. Children who watched more TV were also significantly less physically active (F = 5.16, P = 0.026). Independent of body composition and sex, children with greater physical activity levels had higher TEE (F = 5.15, P = 0.029); however, physical activity did not mediate the relation between TV viewing and adiposity (P > 0.05).
CONCLUSIONS:
Preschool children who watch more TV are fatter and are less active, and activity influences TEE. However, despite TV viewing being linked to lower physical activity, the relation between TV viewing and fatness is not mediated by physical activity. The results suggest that a relation between TV viewing and fatness is more likely to be due to an effect on food intake.

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By Team FPS – April 29, 2012

Metabolism, Brain Size, and Lifespan in Mammals

Also see:
Unsaturated Fats and Longevity
“Curing” a High Metabolic Rate with Unsaturated Fats
Fat Deficient Animals – Activity of Cytochrome Oxidase
Nutrition and Brain Growth in Chick Embryos
PUFA, Development, and Allergy Incidence
W.D. Denckla, A.V. Everitt, Hypophysectomy, & Aging

“A living cell requires energy not only for all its functions, but also for the maintenance of its structure.” -Albert Szent-Gyorgyi

“The length of the life-span, and of the period of youth or immaturity, is closely associated with the size of the brain, and the brain has a very high rate of metabolism. When something interferes with this very high metabolic rate, the consequences may be instantanteous,* or developmental, or chronic and degenerative, or even transgenerational. The issue of epilepsy centers on questions of brain metabolism, and so it has all of those dimensions.” -Ray Peat, PhD

“Besides the observation of greater oxygen consumption in the low fat animals, and high protein tum-over in calorie restricted animals, there are observations in a variety of organisms associating a higher metabolic rate with greater longevity. While most longevity studies of flies involved altering the temperature of their environment, studies of differences of metabolic rate at a given temperature have in several cases found greater longevity in the high metabolizers. A study of 18 strains of mice found a clear association between a higher metabolic rate and greater longevity.(1) Recent studies (e.g., Joseph Graves’) are showing similar associations in
insects.” -Ray Peat, PhD

“Maintaining a high rate of oxidative metabolism, without calorie restriction, retards the accumulation of PUFA, and a high metabolic rate is associated with longevity. An adequate amount of sugar maintains both a high rate of metabolism, and a high respiratory quotient, i.e., high production of carbon dioxide.” -Ray Peat, PhD

“Another factor involved in developing a large brain is the metabolic rate, which is closely associated with the temperature…In birds and mammals, longevity generally corresponds to brain size and metabolic rate.” -Ray Peat, PhD

“They are advancing a myth about human nature, so I will advance a counter-myth. At the time people were growing their large brains they lived in the tropics. I suggest that in this time before the development of grain-based agriculture, they ate a diet that was relatively free of unsaturated fats and low in iron–based on tropical fruits. I suggest that the Boskop skull from Mt. Kilimanjaro was representative of people under those conditions, and that just by our present knowledge of the association of brain size with longevity, they–as various “Golden Age” myths claim–must have had a very long life-span. As people moved north and developed new ways of living, their consumption of unsaturated fats increased, their brain size decreased, and they aged rapidly. Neanderthal relics show that flaxseed was a staple of their diet.” -Ray Peat, PhD

“It has been observed that the ratio of brain weight to body weight corresponds directly to longevity. The brain has a nourishing, trophic influence on other tissues. A stable, efficient brain is an anti-stress agent. The hormones of stress age various tissues, including connective tissue. Good nutrition, including the anti-stress substances found in certain foods, will simultaneously optimize intelligence and increase the healthy life span. Congenital defects are increased by stress and poor nutrition during pregnancy and, conversely, reduced by good nutrition hormone supplementation and stress reduction.” -Ray Peat, PhD

“The brain has a high rate of oxidative metabolism, and so it forms a very large proportion of the carbon dioxide produced by an organism. It also governs, to a great extent, the metabolism of other tissues, including their consumption of oxygen and production of carbon dioxide or lactic acid. Within a particular species, the rate of oxygen consumption increases in proportion to brain size, rather than body weight. Between very different species, the role of the brain in metabolism is even more obvious, since the resting metabolic rate corresponds to the size of the brain. For example, a cat’s brain is about the size of a crocodile’s, and their oxygen consumption at rest is similar, despite their tremendous difference in body size.” -Ray Peat, PhD

Q Rev Biol. 1983 Dec;58(4):495-512.
Energy metabolism, brain size and longevity in mammals.
Hofman MA.
The mathematical relations between basal energy metabolism, brain size, and life span in mammals have been investigated. The evolutionary level of brain development, or encephalization (c), is a function both of brain weight (E) and of body weight (P) according to (formula; see text) Brain weight was found to be a linear function of the product of encephalization and basal metabolic rate. The oxygen consumption of the brain (Mbrain) is proportional to both encephalization and body weight according to (formula; see text) the ratio of metabolic rate in the cerebral cortex to that in the brain as a whole depends solely upon the degree of encephalization and is independent of the size of the animal. The maximum potential life span of a mammal was found to be proportional to the product of its degree of encephalization and the reciprocal of its metabolic rate per unit weight. Life span may be regarded as the algebraic sum of two components: (1) a deduced somatic component (Lb) inversely related to the basal metabolic rate per unit weight, and (2) an encephalization component (Le) related directly to the evolutionary increase of relative brain size.

Experimental Gerontology Volume 2, Issue 3, August 1967, Pages 173–182
Relation of lifespan to brainweight, bodyweight, and metabolic rate among inbred mouse strains
John B. Storer
Mean values for lifespan, brainweight, bodyweight, and metabolic rate were determined for male and female mice in 18 different inbredstrains. No significant correlation between means for log lifespan and log brainweight, log lifespan and log bodyweight, or log brainweight and log bodyweight could be demonstrated. The mean metabolic rate was significantly positively correlated with longevity in both sexes. A component of metabolic rate which is independent of body size may also be positively correlated with longevity.The findings contrast sharply with the between-species correlations of these variables. Possible reasons for this disparity are discussed.

Biol Lett. 2006 December 22; 2(4): 557–560.
Metabolic costs of brain size evolution
Karin Isler* and Carel P van Schaik
In the ongoing discussion about brain evolution in vertebrates, the main interest has shifted from theories focusing on energy balance to theories proposing social or ecological benefits of enhanced intellect. With the availability of a wealth of new data on basal metabolic rate (BMR) and brain size and with the aid of reliable techniques of comparative analysis, we are able to show that in fact energetics is an issue in the maintenance of a relatively large brain, and that brain size is positively correlated with the BMR in mammals, controlling for body size effects. We conclude that attempts to explain brain size variation in different taxa must consider the ability to sustain the energy costs alongside cognitive benefits.

Individuals within a strain of mice were found to vary considerably in their metabolic rate. The 25% of the mice with the highest rate used 30% more energy (per gram of body weight) than the 25% with the lowest metabolic rate, and lived 36% longer (Speakman, et al., 2004). -Ray Peat, PhD

Aging Cell. 2004 Jun;3(3):87-95.
Uncoupled and surviving: individual mice with high metabolism have greater mitochondrial uncoupling and live longer.
Speakman JR, Talbot DA, Selman C, Snart S, McLaren JS, Redman P, Krol E, Jackson DM, Johnson MS, Brand MD.
Two theories of how energy metabolism should be associated with longevity, both mediated via free-radical production, make completely contrary predictions. The ‘rate of living-free-radical theory’ (Pearl, 1928; Harman, 1956; Sohal, 2002) suggests a negative association, the ‘uncoupling to survive’ hypothesis (Brand, 2000) suggests the correlation should be positive. Existing empirical data on this issue is contradictory and extremely confused (Rubner, 1908; Yan & Sohal, 2000; Ragland & Sohal, 1975; Daan et al., 1996; Wolf & Schmid-Hempel, 1989]. We sought associations between longevity and individual variations in energy metabolism in a cohort of outbred mice. We found a positive association between metabolic intensity (kJ daily food assimilation expressed as g/body mass) and lifespan, but no relationships of lifespan to body mass, fat mass or lean body mass. Mice in the upper quartile of metabolic intensities had greater resting oxygen consumption by 17% and lived 36% longer than mice in the lowest intensity quartile. Mitochondria isolated from the skeletal muscle of mice in the upper quartile had higher proton conductance than mitochondria from mice from the lowest quartile. The higher conductance was caused by higher levels of endogenous activators of proton leak through the adenine nucleotide translocase and uncoupling protein-3. Individuals with high metabolism were therefore more uncoupled, had greater resting and total daily energy expenditures and survived longest – supporting the ‘uncoupling to survive’ hypothesis.

FASEB J. 14, A757
Living fast and dying old: cross sectional variation in daily energy expenditure is positively linked to lifespan in female mice.
Speakman, J. R.; Snart, S.; Selman, C.; McLaren, J. S.; Redman, P.; Krol, E.; Jackson, D. M.; Johnson, M. S.
Inter-relationships between metabolism and longevity are confused. On one hand, inter-specific studies point to a strong negative relationship. Yet comparisons across classes yield the opposite trend. No previous studies have examined the consequences for lifespan of intraspecific variations in energy expenditure of animals living in a constant environment. Here, we report such a study in a group of 42 female MF1 mice. Between 6 and 13 months of age we monitored food intake, daily energy expenditure and assimilation efficiency. After 13 months of age, the mice were monitored daily until they died. We sought relationships between lifespan and the traits measured when the mice were 6-13-months-old. Contrary to expectations there were significant positive relationships between lifespan and daily energy expenditure, residual energy expenditure and metabolic intensity (energy expenditure per gram body mass). In this cohort of mice, living fast was associated with dying more slowly.

J Nutr. 2002 Jun;132(6 Suppl 2):1583S-97S.
Living fast, dying when? The link between aging and energetics.
Speakman JR, Selman C, McLaren JS, Harper EJ.
The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die. Evidence supporting the “rate-of-living” theory was gleaned from the scaling of resting metabolism and life span as functions of body mass. The product of these factors yields a mass-invariant term, equivalent to the “amount of living.” There are at least four problems with this evidence, which are summarized and reviewed in this communication: 1) life span is a poor measure of aging, 2) resting metabolism is a poor measure of energy expenditure, 3) the effects are confounded by body mass and 4) the comparisons made are not phylogenetically independent. We demonstrate that there is a poor association between resting metabolic rate (RMR) and daily energy expenditure (DEE) measured using the doubly labeled water (DLW) method at the level of species. Nevertheless, the scaling relation between DEE and body mass still has the same scaling exponent as the RMR and body mass relationship. Thus, if we use DEE rather than RMR in the analysis, the rate-of-living ideas are still supported. Data for 13 species of small mammal were obtained, where energy demands by DLW and longevity were reliably known. In these species, there was a strong negative relationship between residual longevity and residual DEE, both with the effects of body mass removed (r(2) = 0.763, F = 32.1, P < 0.001). Hence, the association of energy demands and life span is not attributed to the confounding effects of body size. We subjected these latter data to an analysis that extracts phylogenetically independent contrasts, and the relationship remained significant (r(2) = 0.815, F = 39.74, P < 0.001). Small mammals that live fast really do die young. However, there are very large differences between species in the amounts of living that each enjoy and these disparities are even greater when other taxa are included in the comparisons. Such differences are incompatible with the “rate-of-living” theory. However, the link between energetics and aging across species is reconcilable within the framework of the “free-radical damage hypothesis” and the “disposable soma hypothesis.” Within species one might anticipate the rate-of-living model would be more appropriate. We reviewed data generated from three different sources to evaluate whether this were so, studies in which metabolic rate is experimentally increased and impacts on life span followed, studies of caloric restriction and studies where links between natural variation in metabolism and life span are sought. This review reveals that there might be contrasting effects of resting and nonresting energy expenditure on aging, with increases in the former being protective and increases in the latter being harmful.

Many dog owners are aware that small dogs eat much more food in proportion to their size than big dogs do. And small dogs have a much greater life expectancy than big dogs, in some cases about twice as long (Speakman, 2003). -Ray Peat, PhD

Aging Cell. 2003 Oct;2(5):265-75.
Age-related changes in the metabolism and body composition of three dog breeds and their relationship to life expectancy.
Speakman JR, van Acker A, Harper EJ.
We measured body composition and resting metabolic rates (RMR) of three dog breeds (Papillons, mean body mass 3.0 kg (n = 35), Labrador retrievers, mean body mass 29.8 kg (n = 35) and Great Danes, mean body mass 62.8 kg (n = 35)) that varied between 0.6 and 14.3 years of age. In Papillons, lean body mass (LBM) increased with age but fat mass (FBM) was constant; in Labradors, both LBM and FBM were constant with age, and in Great Danes, FBM increased with age but LBM was constant. FBM averaged 14.8% and 15.7% of body mass in Papillons and Labradors, respectively. Great Danes were leaner and averaged only 10.5% FBM. Pooling the data for all individuals, the RMR was significantly and positively associated with LBM and FBM and negatively associated with age. Once these factors had been taken into account there was still a significant breed effect on RMR, which was significantly lower in Labradors than in the other two breeds. Using the predictive multiple regression equation for RMR and the temporal trends in body composition, we modelled the expenditure of energy (at rest) over the first 8 years of life, and over the entire lifespan for each breed. Over the first 8 years of life the average expenditure of energy per kg LBM were 0.985, 0.675 and 0.662 GJ for Papillons, Labradors and Great Danes, respectively. This energy expenditure was almost 60% greater for the smallest compared with the largest breed. On average, however, the life expectancy for the smallest breed was a further 6 years (i.e. 14 years in total), whereas for the largest breed it was only another 6 months (i.e. 8.5 years in total). Total lifetime expenditure of energy at rest per kg LBM averaged 1.584, 0.918 and 0.691 GJ for Papillons, Labradors and Great Danes, respectively. In Labradors, total daily energy expenditure, measured by the doubly labelled water method in eight animals, was only 16% greater than the observed RMR. High energy expenditure in dogs appears positively linked to increased life expectancy, contrary to the finding across mammal species and within exotherms, yet resembling observations in other intra-specific studies. These contrasting correlations suggest that metabolism is affecting life expectancy in different ways at these different levels of enquiry.

J Exp Biol. 2005 May;208(Pt 9):1717-30.
Body size, energy metabolism and lifespan.
Speakman JR.
Bigger animals live longer. The scaling exponent for the relationship between lifespan and body mass is between 0.15 and 0.3. Bigger animals also expend more energy, and the scaling exponent for the relationship of resting metabolic rate (RMR) to body mass lies somewhere between 0.66 and 0.8. Mass-specific RMR therefore scales with a corresponding exponent between -0.2 and -0.33. Because the exponents for mass-specific RMR are close to the exponents for lifespan, but have opposite signs, their product (the mass-specific expenditure of energy per lifespan) is independent of body mass (exponent between -0.08 and 0.08). This means that across species a gram of tissue on average expends about the same amount of energy before it dies regardless of whether that tissue is located in a shrew, a cow, an elephant or a whale. This fact led to the notion that ageing and lifespan are processes regulated by energy metabolism rates and that elevating metabolism will be associated with premature mortality–the rate of living theory. The free-radical theory of ageing provides a potential mechanism that links metabolism to ageing phenomena, since oxygen free radicals are formed as a by-product of oxidative phosphorylation. Despite this potential synergy in these theoretical approaches, the free-radical theory has grown in stature while the rate of living theory has fallen into disrepute. This is primarily because comparisons made across classes (for example, between birds and mammals) do not conform to the expectations, and even within classes there is substantial interspecific variability in the mass-specific expenditure of energy per lifespan. Using interspecific data to test the rate of living hypothesis is, however, confused by several major problems. For example, appeals that the resultant lifetime expenditure of energy per gram of tissue is ‘too variable’ depend on the biological significance rather than the statistical significance of the variation observed. Moreover, maximum lifespan is not a good marker of ageing and RMR is not a good measure of total energy metabolism. Analysis of residual lifespan against residual RMR reveals no significant relationship. However, this is still based on RMR. A novel comparison using daily energy expenditure (DEE), rather than BMR, suggests that lifetime expenditure of energy per gram of tissue is NOT independent of body mass, and that tissue in smaller animals expends more energy before expiring than tissue in larger animals. Some of the residual variation in this relationship in mammals is explained by ambient temperature. In addition there is a significant negative relationship between residual lifespan and residual daily energy expenditure in mammals. A potentially much better model to explore the links of body size, metabolism and ageing is to examine the intraspecific links. These studies have generated some data that support the original rate of living theory and other data that conflict. In particular several studies have shown that manipulating animals to expend more or less energy generate the expected effects on lifespan (particularly when the subjects are ectotherms). However, smaller individuals with higher rates of metabolism live longer than their slower, larger conspecifics. An addition to these confused observations has been the recent suggestion that under some circumstances we might expect mitochondria to produce fewer free radicals when metabolism is higher–particularly when they are uncoupled. These new ideas concerning the manner in which mitochondria generate free radicals as a function of metabolism shed some light on the complexity of observations linking body size, metabolism and lifespan.

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By Team FPS – April 29, 2012