Friday, 3 June 2011

Raw Chia Seed Pudding Parfait


Joanne over at Foods For Long Life created this absolutely delicious Raw Chia Seed Pudding with Cinnamon. I made it exactly as her recipe shows and then added one cup of raspberries and blueberries to make a yummy parfait for lunch. I did not add any sugar to the berries. You definately want to give this recipe a try.  My taste testers loved it too!!  Joanne is also doing "One Week of Raw and Gluten Free" recipes.  She has an Anti-Aging Smoothie, Faux Tuna Salad, Macadamia Mango Blast Smoothie and much , much more. Her recipes are awesome!!

CHIA SEED FACTS:
  • Chia seeds have an optimal amount of essential Omega-3 and Omega-6 fatty acids in an ideal ratio of 3:1. Omega-3's promote cardiovascular health and may help regulate cholesterol levels, blood pressure, and blood sugar levels. Highest vegetarian source of Omega-3's (gram for gram).
  • Richest Known Whole Food Source of Fiber
  • One serving of chia seeds provides 20% of the daily recommended intake of fiber. Chia contains insoluble and soluble fiber, which may assist in helping to lower cholesterol and blood sugar levels, as well as aid with digestion, detoxification and weight loss.
  • 20% more fiber than flax seeds (gram for gram).
  • High Quality Protein
  • Chia seeds are a vegetarian source of high quality protein containing all the essential amino acids. Proteins are the building blocks of bones, muscles, cartilage, skin, and bones.
  • 3 times more protein than beans and legumes (gram for gram).
Raw Chia Seed Pudding with Cinnamon

Printable Recipe
Makes 4 servings
Raw Vegan, Gluten Free

1/2 cup raw cashews, soaked for 4 to 6 hours and rinsed
3 pitted, jumbo Medjool dates soaked for 4 to 6 hours in 2 cups of water (reserve soak water)
1 teaspoon of vanilla
1/2 teaspoon of cinnamon plus extra for topping
1 packet of stevia (optional for added sweetness)
1/4 cup chia seeds

Place cashews, dates, date soak water, vanilla, cinnamon and stevia in a high speed blender. Blend until smooth and creamy.
In a 1 quart bowl, combine cashew mixture with the chia seeds and stir vigorously with a fork for several minutes.
Let mixture sit for 15 minutes and stir vigorously again until the chia seeds are well blended and no longer clump together.
Once the mixture is well combined and no longer separating, place in the refrigerator for one day.
Dust with more cinnamon and serve.

Per serving: 173.5 calories, 9.1 g fat, 1.3 g saturated fat, 1.8 g omega 3 and 1.7 g omega 6 fatty acids, 0 mg cholesterol, 4.1 g protein, 21.9 g carbohydrate and 5.8 g dietary fiber.

Thursday, 2 June 2011

Bupropion Fails to Aid Hospitalized Smokers with Heart Disease

Smoking and nicotine dependence increase rates for heart disease in the general population. Among those with heart disease, continued smoking increases mortality rates. Targeting smoking cessation efforts at those with heart disease (secondary prevention)is an important clinical challenge.
 
Most of the research data related to drugs for smoking cessation come from subjects recruited from the general population. Both bupropion (Zyban)and varenicline (Chantix)are FDA-approved drugs for smoking cessation in the United States. There is limited data of the safety and effectiveness of these two compounds in those with heart disease.

Dr. David Planer and colleagues from Israel recently published a randomized clinical trial of smokers admitted to the hospital with acute coronary syndrome (myocardial infarction or unstable angina). Subjects in this study were required to have the intent to stop smoking. Subjects received either placebo or bupropion sustained release 300 mg daily. All subjects also received five sessions of smoking cessation counseling from a nurse or physician. These counselors had some previous experience in smoking cessation and received additional training from a smoking cessation counselor prior to the trial.

Unexpectedly, bupropion failed to provide an additional increase in abstinece compared to placebo with the following rates noted at several study time points (Bupropion Bold followed by (Placebo) rates:
  • 3 months: 44% (43%)
  • 6 months: 37% (42%)
  • 12 months: 31% (33%) 
What is striking about these outcome comparisons in the rate of placebo response. The authors note nicotine dependence has one of the lowest rates of placebo response with studies commonly reporting placebo response rates as low as 10% at one year. It is possible that the effect of physician or nurse directed counseling at the time of hospitalization (when motivation may be highest)is quite powerful. This may be the most important finding from the study and provide impetus for more wide spread adoption of this strategy in clinical settings.

Interestingly, one predictor of smoking cessation at one year in this study was undergoing a cardiac procedure (angiography or coronary artery bypass graft) during the hospitalization (odds ratio 4.2, p value=.02). The authors hypothesize that undergoing an invasive procedure may potentiate the psychological distress of the hospitalization and increase motivation for smoking cessation to limit the risk of future procedures and hospitalizations. Previous outcome studies in alcoholism have found that a serious medical problem related to drinking (and the need to be abstinent to address this medical problem) is one of the strongest predictors of alcohol abstinence.

I think this study can not be interpreted to mean there is no place for bupropion in smoking cessation in those hospitalized with coronary artery disease. Coronary artery disease patients hospitalized in facilities with smoking cessation counseling resources may be better off with initiaion of bupropion or another smoking cessation drug. The study did find bupropion to be safe and generally well tolerated in this population. Bupropion might be a reasonable choice for smokers who experience depression in the course of the heart disease.

Physicians should see this study as an example of the power of their words and efforts in smoking cessation. Strongly urging smoking cessation in a place and time where it is most likely to be effective is crucial. Missing such opportunities may contribute to continued progression of heart disease and other smoking-related medical problems.

Photo of Cattle Egret from Maui Hawaii Courtesy of Yates Photography
Planer, D., Lev, I., Elitzur, Y., Sharon, N., Ouzan, E., Pugatsch, T., Chasid, M., Rom, M., & Lotan, C. (2011). Bupropion for Smoking Cessation in Patients With Acute Coronary Syndrome Archives of Internal Medicine DOI: 10.1001/archinternmed.2011.72

Wednesday, 1 June 2011

Ray Peat - PUFA

It’s time for the Ray Peat finale. Yeah I know, it’s a day late. I moved out of my apartment yesterday and didn’t have enough mojo left to work on it. Anyway, we’ll pick up where we left off in the last Peat article. If you know anything about Peat, know that he has a vendetta against polyunsaturated fat – which could very well be his greatest scientific contribution because of the numerous negative actions that excessive polyunsaturated fat intake exerts on human tissues, organs, and glands like the wondrous thyroid.


"The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do (Fu, et al., 1996). And the oxidation of fats rather than glucose means that the proteins won't have as much protective carbon dioxide combined with their reactive nitrogen atoms, so the real difference in the organism is likely to be greater than that seen by Fu, et al."

You hear low-carbers freaking out about raising blood sugar because it causes glycation of proteins similar to what grilling does to a juicy steak. Of course, eating carbohydrates does not raise blood sugar significantly in a healthy person – and all the focus should be on restoring insulin sensitivity and not avoiding glucose. In fact, one person contacted me last week to share with me a dramatic lowering of blood glucose levels and complete conquering of pretty severe insulin resistance after quadrupling carbohydrate intake – a result of eating a high-starch, low polyunsaturated fat diet. Several years of low-carbing gave her extremely high insulin levels (14-18 iu/M), which dropped to 4.7 in four months of RRARF.

Anyway, that aside, Peat points out that polyunsaturated fatty acids are a much more major culprit in protein glycation than glucose. That rings true for me, as I reversed many signs of aging years ago on a high sugar diet, but seemed to age much more quickly during my years on a low-carb diet, which featured lots of high-PUFA pork, poultry, and total polyunsaturated fat intake (hard to avoid when eating 200-300 grams of fat per day).

"These products of lipid peroxidation, HNE, MDA, acrolein, glyoxal, and other highly reactive aldehydes, damage the mitochondria, reducing the ability to oxidize sugar, and to produce energy and protective carbon dioxide."

Basically the polyunsaturated fats, because they are more heat, oxygen, and light sensitive – degrade much more quickly in the human body. Although certainly better, in the grand scheme of things it probably doesn’t matter if you eat your PUFA with a bunch of vitamins, minerals, and antioxidants or not. When tissues are comprised of polyunsaturated fats they will simply deteriorate and age you more quickly. That’s just how it goes. And because of the byproducts of their degradation, glucose metabolism is eventually impaired – leading to insulin resistance, metabolic syndrome, and type 2 diabetes.

"Fish oil, which is extremely unstable in the presence of oxygen and metals such as iron, produces some of these dangerous products very rapidly. The polyunsaturated “essential fatty acids” and their products, arachidonic acid and many of the prostaglandin-like materials, also produce them."

Peat is very controversial when it comes to fish oil. While we know that there are countless anti-inflammatory benefits to mega-dosing fish oil in the short-term, Peat seems unfazed. He knows that the more fish oil you have in your tissues, the more quickly you will deteriorate. I think Peat would look at fish oil as a get-health-quick scheme that is a terrible long-term investment.

"Brief exposures to polyunsaturated fatty acids can damage the insulin-secreting cells of the pancreas, and the mitochondria in which oxidative energy production takes place. Prolonged exposure causes progressive damage. Acutely, the free polyunsaturated fatty acids cause capillary permeability to increase, and this can be detected at the beginning of “insulin resistance” or “diabetes.” After chronic exposure, the leakiness increases and albumin occurs in the urine, as proteins leak out of the blood vessels. The retina and brain and other organs are damaged by the leaking capillaries."

When I talk about polyunsaturated fat, I usually focus on the anti-metabolic effects of the fats. Peat’s research goes far beyond this to include the various ways they can do damage to tissues, blood vessels, and so forth.

"The blood vessels and other tissues are also damaged by the chronically increased cortisol, and at least in some tissues (the immune system is most sensitive to the interaction) the polyunsaturated fats increase the ability of cortisol to kill the cells."

Like I’ve said before, loading up the tissues with polyunsaturated fat is like giving a sniper a nuclear bomb to take out threats in which a simple long range rifle would have been sufficient. Collateral damage. Yes that's the name of an Arnold movie, and no his love of fairly unattractive maids cannot deter me from worshipping the Sperminator. I know Maria probably eats nothing but salad, and consequently has the sex drive of a panda. She knew what she was getting into. Arnold needs to be coming day and night! This video is even funnier given the recent fiASSco…



"When cells are stressed, they are likely to waste glucose in two ways, turning some of it into lactic acid, and turning some into fatty acids, even while fats are being oxidized, in place of the sugar that is available. Growth hormone and adrenalin, the stress-induced hormones, stimulate the oxidation of fatty acids, as well as their liberation from storage, so the correction of energy metabolism requires the minimization of the stress hormones, and of the free fatty acids. Prolactin, ACTH, and estrogen also cause the shift of metabolism toward the fatty acids."

This translates to resting up and eating a high-carb, high-calorie, low-PUFA diet with a little added fat and protein and frequent feedings. It’s amazing what something so simple can do for glucose metabolism and subsequent health improvements that stem from an impairment in glucose metabolism.

"Sugar and thyroid hormone (T3, triiodothyronine) correct many parts of the problem. The conversion of T4 into the active T3 requires glucose, and in diabetes, cells are deprived of glucose. Logically, all diabetics would be functionally hypothyroid. Providing T3 and sugar tends to shift energy metabolism away from the oxidation of fats, back to the oxidation of sugar."

The lack of glucose is one reason metabolism falls so sharply on low-carbohydrate diets, and why it takes a common root problem (hypothyroidism) and makes it worse. You can also see why having a higher metabolic rate would prevent insulin resistance and keep glucose oxidation firing on all cylinders. Type 2 diabetes could be described as an inability to use glucose properly, not a disease of consuming too much sugar. In fact, eating more carbohydrate improves the ability of your body to use glucose properly – generally-speaking.

"Sodium, which is lost in hypothyroidism and diabetes, increases cellular energy. Diuretics, that cause loss of sodium, can cause apparent diabetes, with increased glucose and fats in the blood. Thyroid, sodium, and glucose work very closely together to maintain cellular energy and stability."

The vendetta that the mainstream has against sodium could be very inappropriate considering the low metabolic rate of the masses. In fact, eating more salt and more carbohydrate could be a more appropriate recommendation to give to a hypothyroid population. When looking at the origins of many of our common diseases with an open mind as Peat and I have, a very different picture emerges.

"In Houssay's experiments, sugar, protein, and coconut oil protected mice against developing diabetes. The saturated fats of coconut oil are similar to those we synthesize ourselves from sugar. Saturated fats, and the polyunsaturated fats synthesized by plants, have very different effects on many important physiological processes. In every case I know about, the vegetable polyunsaturated fats have harmful effects on our physiology."

Aside from his controversial statement about Houssay’s experiments, Peat is basically saying that human biology – and all mammalian biology with maybe the exception of hibernating animals that derive a massive benefit from the anti-metabolic polyunsaturated fats in autumn, favors saturated fats over polyunsaturated fats – or at the very least a high ratio of saturated to unsaturated fat. That is the case with virtually all mammalian milk and also the type of fats that are produced inside the body as well. While many adhere stubbornly to a simple-minded “if it’s natural it HAS to be good” philosophy, it could very well be that there are natural things that are more congruent, and natural things that are less congruent, with our general and individual physiological makeup. There can be better and worse options. Not all things are created equal.

"For example, they bind to the “receptor” proteins for cortisol, progesterone, and estrogen, and to all of the major proteins related to thyroid function, and to the vesicles that take up nerve transmitter substances, such as glutamic acid."

In other words, polyunsaturated fats interfere with normal hormone action, including impairing the effectiveness of the thyroid hormones. This is significant, as you could have normal or even above-normal thyroid hormone production (or other hormones) and still be deficient at the cellular level.

"Unsaturated fatty acids activate the stress hormones, sugar restrains them."

That is the crux of Peat’s belief system right there.

"The protective effects of sugar, and the harmful effects of excessive fat metabolism, are now being widely recognized, in every field of physiology. The unsaturated vegetable fats, linoleic and linolenic acid and their derivatives, such as arachidonic acid and the long chain fish oils, have excitatory, stress promoting effects, that shift metabolism away from the oxidation of glucose, and finally destroy the respiratory metabolism altogether. Since cell injury and death generally involve an imbalance between excitation and the ability to produce energy, it is significant that the oxidation of unsaturated fatty acids seems to consume energy, lowering cellular ATP (Clejan, et al, 1986)."

While Mark Sisson is calling excessive “fat metabolism” a paradigm shift – claiming it is superior, I don’t know if anything could convince me of this after my experience with a slow and steady degradation of health on a high-fat, near-zero sugar diet. Peat claims that it is recognized in “every field of physiology” that glucose oxidation is superior to fat. I don’t know about this.

"The bulk of the age-related tissue damage classified as “glycation end-products” (or “advanced glycation end-products,” AGE) is produced by decomposition of the polyunsaturated fats, rather than by sugars, and this would be minimized by the protective oxidation of glucose to carbon dioxide."

Once again, Peat is casting the blame of glycation on decomposition of polyunsaturated fats more so than exposure to high levels of glucose.

"Protein of the right kind, in the right amount, is essential for reducing stress. Gelatin, with its antiinflammatory amino acid balance, helps to regulate fat metabolism."

I had hoped to talk more about gelatin, but there’s really not that much to say about it other than the amino acid profile of gelatin, because it lacks methionine, cysteine, and tryptophan, tends to have a more anti-inflammatory effect. I’m not sure it is clear what the right kind and amount of protein truly is. It probably is very different for each species, and is highly dependent on activity levels, gender, age, and the context of the rest of the diet. But in the interest of improving glucose oxidation I don’t think there’s any question that eating more calories and more of those calories as carbohydrates – sugar, starch, or a blend of the two, achieves that effect in addition to reducing the overall protein requirement. “Animal” protein is fantastic for muscle-building and during the growth and development phases of life – which is why dairy and eggs for example are so rich in growth-promoting proteins. But otherwise plant proteins seem to keep inflammation much lower. I haven’t found a faster way to reduce inflammation personally or with my own family members than to reduce animal protein ingestion.

Anyway, we’ll let that conclude our month of Ray Peat. You should be pretty sick of Ray Peat by now and ready to move on. But it is important to see where he is coming from, particularly as it pertains to polyunsaturated fat.

When nearly every disease state we know of is being increasingly linked to inflammation, free radical production, and low mitochondrial activity – and the links between each one of the “Big 3” you might call them are clearly negatively impacted by excess polyunsaturated fat intake (which also happens to be the most dramatic dietary change that took place in the 20th century), Peat’s smear campaign against them becomes incredibly valuable and timely. There is no doubt that he is one of the greatest contributors to the understanding of the nutrition-health interaction of any researcher that has come before him. I hope we can continue to learn from him, while also building on his work – better refining and individualizing it in the future. Yay Ray!

www.raypeat.com


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HUP's Pups is a Hit

The Hospital of the University of Pennsylvania’s (HUP) new animal-assisted therapy program, HUP’s Pups, has been a hit with both patients and staff. Research shows patient interaction with animals offers physiological benefits including decreased heart rate and blood pressure. All animal volunteers at Penn Medicine and their handlers are certified by professional pet therapy organizations, including the Delta Society and Therapy Dogs International.

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Fiber Up! Dietary Fiber and Mortality Risk

We hear quite a bit in the lay press about the potential benefits of dietary fiber including eating multiple daily servings whole grains,  fruits and vegetables.  I tend to be skeptical of many of these recommendations.  But after following some of the research related to the Mediterranean Diet,  I at least have my antenna (and my Google Reader) up on this issue.  A previous post on basics of the Mediterranean diet is here and a review of a study linking the diet to slower cognitive decline in older adults is here.

My Google Reader recently retrieved an online first article from the Archives of Internal Medicine by Dr. Park and colleagues from the National Cancer Institute entitled "Dietary Fiber Intake and Mortality in the NIH-AARP Diet and Health Study". 

This is a longitudinal correlational study of the association between self-reported dietary fiber intake and cause of death from the National Death Index Plus registry.  I wasn't aware of this study that includes cooperation with the American Association of Retired Persons or AARP.  AARP collaborated with the National Institute of Health on a survey completed by 567, 169 AARP members in 1995 and 1996.

The survey collected detailed personal dietary habit information and then scanned the National Death Index for deaths in those who had completed the survey.   The daily dietary fiber intake was calculated for each participant and split into quintiles (five groups each comprised of 20% of the sample) with those with the highest fiber intake (top 20%) compared to those with the lowest fiber intake (lowest 20%).  Rates of death for these two groups were examined.  Since people who tend to eat more nutritious diets tend to also have other healthy lifestyle behaviors, a variety of potential confounding variables were controlled, i.e. smoking status, age, race, education, marital status, baseline health status, alcohol consumption, etc.

During the follow up period, here is the estimated reduced death rates associated with being in the highest fiber intake groups (compared to lowest) with women in bold first followed (men):
  • Death from cardiovascular disease: 34% lower (24% lower)
  • Death from cancer: 4% (not statistically significant) lower, (17% lower)
  • Death from respiratory disease: 46% lower, (41% lower)
  • Death from infectious disease: 69% lower, (56% lower)
Risk of death from accidents did not differ by dietary fiber ranking.  However, the study numbers are pretty impressive.  Although there is pretty good data supporting dietary fiber and cardiovascular disease risk, there is limited study in other causes of death.  This study supports association between dietary fiber and lower cancer deaths in men, but not women.  The authors point out that many of the types of male-predominant cancers (i.e. head and neck, esophageal, liver, bladder and kidney) may be those where dietary fiber plays a role.  Another potential interpretation is that breast cancer is not influenced by dietary fiber.

I was surprised by the finding of reduced death in the respiratory and infectious disease categories.  There were many fewer deaths in these categories so the results need to be interpreted cautiously.  However, there is at least one study (Iowas Women's Health Study) showing dietary fiber reduced death from inflammatory disorders.  The authors point out something I didn't know, that high dietary fiber is associated with reduced levels of endogenous (the body's own) inflammation markers including lower C-reactive protein, interleukin 6 and tumor necrosis factor alpha receptor.  Inflammation may play a role in deaths due to asthma and other lung inflammatory conditions.

This study provides some additional intriguing data.  The authors broke down the source of dietary fiber into whole grains, vegetables, fruits and bean sources.  What they found was that the dietary fiber from grains (but not fiber from vegetables, fruits or beans) contributed the largest effect of the association of high fiber intake with reduced mortality.  And this is where the figure above comes in.  The figure shows that in a whole wheat kernel, the wheat bran and wheat germ pack the most fiber, minerals and chemicals called phytochemicals.  The authors propose that high dietary grain fiber is likely to include high intake of whole grain components such as wheat bran and wheat germ.

Again, these findings are only correlational.  They do not prove a cause and effect.  There may be some other factor contributing to this reduced mortality in the high fiber group.  This study does not prove putting people with a low fiber diet on a high fiber diet will reduce their risk of death during a period of follow up.  But my skepticism is fading so please excuse me now as I'm heading to the store for some bran cereal and a box of rolled oats.

Disclosure: I had not reached the minimum age for AARP membership in 1995 and did not participate in this survey.  I am now an AARP member primarily for motel/hotel discounts for AARP members.  I received no money from AARP, the American Bean Council or other source for writing this post. 

The figure in this post comes from Wikipedia Commons file authored by jkwchui.

Park, Y., Subar, A., Hollenbeck, A., & Schatzkin, A. (2011). Dietary Fiber Intake and Mortality in the NIH-AARP Diet and Health Study Archives of Internal Medicine DOI: 10.1001/archinternmed.2011.18