Resveratrol blocks weight gain in primate study

Gray mouse lemur

Resveratrol—a natural red-wine compound previously shown to protect mice against excess weight gain when fed a high-fat diet—has now been found to reduce seasonal weight gain in gray mouse lemurs in a primate model of obesity.

The study was published in BMC Physiology by a team of researchers from the Centre Nationale de la Recherche Scientifique, Museum National d’Histoire Naturelle, of Paris, who wrote that they had “demonstrated for the first time the short-term effects of resveratrol on the metabolism of an heterothermic [with varying body temperatures] primate.”

Gray mouse lemurs are a species of prosimian primate that can double in weight (seasonal fattening) within a matter of weeks. This increase in energy reserves is induced by the arrival of shorter days and longer nights (shorter photoperiod), which serves as a means of adapting to the long dry winters in its natural environment in Madagascar.

When given four weeks of resveratrol supplementation at the time of pre-winter fattening (200 milligrams per kilogram per day), the gray mouse lemurs exhibited the following “significant effects on energy metabolism”:

Reduction in seasonal body-mass gain associated with an increase in resting metabolic rate of 29 percent while decreasing food calorie intake by 13 percent.

Strong reduction of daily heterothermia expression (changes of body temperature relating to season) with no change in the daily amount of locomotor activity.

An increased secretion of glucose-dependent insulinotropic polypeptide (a gut hormone known to induce insulin secretion) levels that may play an additive role in limiting body-mass gain.

The researchers concluded that, “resveratrol activates energy expenditure by inducing an increase in resting metabolic rate and a decrease in torpor [temporary hibernation] patterns that play key roles in energy saving in this primate. Moreover, resveratrol had a satiety effect in this primate that reduced their spontaneous food intake.”

Resveratrol’s effects are potentially due to stimulation of SIRT1, one of family of sirtuin enzymes, that has a direct role in fat metabolism. Calorie restriction and, recently, intermittent fasting have also been shown to activate SIRT1 activity.

Mouse Lemurs to Humans

In a prepared statement, Fabienne Aujard, a co-author of the study, wrote, “The physiological benefits of resveratrol are currently under intensive investigation, with recent work suggesting that it could be a good candidate for the development of obesity therapies.”

When asked through e-mail about how the study related to humans, Aujard replied that the main point of the study is that the gray mouse lemur is a non-human primate, “This species is genetically closer to human. The data obtained with this lemur should be more easily extrapolated to humans compared to rodent studies.”

Investigation conducted in humans have mainly studied bioavailability in lesser amounts, not in the high amounts given to the lemurs (equivalent of a human weighing 70 kilograms taking 14 grams of resveratrol). At present, the maximum single dose studied in humans has been 5 grams (70 milligrams per kilogram for a human of 70 kilograms).

“However, despite being a primate, the mouse lemur’s organism is certainly very different from that of a human because of its size and its seasonality,” writes Aujard. “The mouse lemur is a small animal and, like all small mammals, it has a very active metabolism, thus, a very important nutrient metabolism. Therefore, we believe that the doses to be ingested by human to reach the same long-term effects will certainly be lower than that given to lemurs.”

The general recommendation for humans is between 50 to 500 milligrams daily, which is safe as supported by human clinical studies. Although this study shows promising results, it is not yet known whether or not resveratrol will influence fat metabolism or body composition in humans.

Source: Dal-Pan A, Blanc S, Aujard F. Resveratrol suppresses body mass gain in a seasonal non-human primate model of obesity. BMC Physiol 2010;10:11.

If You Ever Had Doubts About Our Ancestors Eating Shellfish, See Curtis Marean's Feature

When the Sea Saved HumanityPowered by Ergo:Ux

Anti-Aging with Aubrey de Grey

A couple of weekends ago I was in LA going to a meet-up with biomedical gerontologist Aubrey de Grey to discuss new research on aging. He talked about a new paper he co-authored with a few of his other biogerontologist colleagues.

So, I asked him to tell me more. Out of that meeting came a follow-up interview and this article published on KurzweilAI.net. Please read that article as it describes well why we must prevent a "Global Aging Crisis".

And for anyone who wants to read the entire interview with Aubrey and the efforts of the SENS Foundation, here it is below:

Q. Would you give a brief summary of the new paper of which you are listed as a co-author in Science Translational Medicine?

The essence of this paper is that we argue for a more balanced approach to the quest for interventions to postpone age-related ill-health. Specifically, we highlight the fact that there are three general strategies to consider:

- promotion of healthy lifestyles (through reduction in environmental toxins, medical control of disease risk factors, etc);

- interventions to slow down the lifelong aging process, i.e. the accumulation of various types of molecular and cellular damage that eventually contribute to age-related pathology; and

- interventions to repair that damage using (broadly defined) regenerating medicine

and we highlight the features and limitations of each approach. Our main conclusion, as reflected in the paper's title, is that there is a atrong case for increasing the emphasis on the "damage-repair" style of intervention, which hitherto has received much less attention from gerontologists and policy-makers than the others.

Q. Who are the other authors on the review and why is it meaningful to have them come together with you to co-author this paper?

Five of the other authors - Butler, Campisi, Finch, Martin and Vijg - are among the absolute top tier of biogerontologists, whose views are universally respected within the field. They have never previously expressed the above conclusion (or not nerly so unequivocally), even individually. Therefore, their voice here will make a huge impact on thinking about this issue, both within the field and beyond. Another author, Gough, is a policy veteran with great influence in the corridors of power. The remaining authors - Rae, Perrott and Logan - are involved in organisations that have been promoting the case for repair-style interventions for some years.

Q. What impact will this paper have on the SENS Foundation? Do you expect the paper to raise more awareness and possible funding for research into "pre-disease interventions" and "human regenerative engineering"?

I feel very confident that this will be of great benefit to SENS Foundation, yes. SENSF is the global spearhead of the application of regenerative medicine to aging, and we intend to leverage this paper considerably.

Q. Could you briefly describe "pre-disease interventions" and "human regenerative engineering" as addressed in your paper?

We don't go into many details in this paper concerning the specifics of the interventions, but in my work over the past decade I have identified seven major categories of molecular and cellular "damage" that I believe we need to repair (or in some cases obviate) in order to rejuvenate the aged body comprehensively, and ways to implement that repair. Very briefly, the interventions consist of stem cell therapies to combat cell loss, suicide gene therapy against death-resistant cells, non-human enzymes against intracellular "molecular garbage", vaccination against extracellular "molecular garbage", small-molecule drugs against spontaneous crosslinks in the extracellular matrix, nuclear copies of the mitochondrial DNA to obviate mitochondrial mutations, and a complex combination therapy (involving suppression of telomere elongation together with a variety of stem cell therapies) to pre-empt cancer.

Q. Many gerontologists do not share your ideals about ending aging, how does the new paper seek to change paradigms? What paradigm is ideal in gerontology?

The ideal is not to have only one paradigm. Those gerontolgists who favour "optimising metabolism" to slow down the creation of these various types of molecular and cellular damage, rather than regenerative medicine to repair the damage, are not wrong: their approach is intrinsically less powerful, but it's also very likely to be far easier to implement. As such, it provides a "bridge" to the regenerative approach; the greatest benefit to humanity in terms of lives saved and suffering averted will occur if both approaches are pursued equally aggressively.

Q. What is human healthspan extension? How is this different than life extension?

For practical purposes there is no difference, and this is something that needs to be understood far better by the general public and by policy-makers. We simply cannot plausibly extend lifespans very much by keeping people alive in the diminished state of health that most people currently endure for the last year or three of their lives. Significant life extension will therefore occur only if we can postpone age-related ill-health, i.e. extend the healthy part of our lives. With regenerative medicine, I believe we have a realistic prospect of postponing ill-health so well that we simply never attain it - we postpone it faster than time is passing.

Q. Why do you think more people in general need to become familiar with new paradigms such as human healthspan extension? How will this new paper seek to break pre-conceived notions about aging?

The core reason is the obvious, boring one: funding. Serious public-purse resources to develop regenerative medicine against aging will emerge only when there is public support for it, and that will occur only by educating the respected, mainstream scientific community to take the concept seriously. This paper is directed mainly at those people - the biogerontologists who have hitherto presumed that this approach is too difficult to be worth even considering, or who have not appreciated its potential.

Q. What advice would you give to university students and scientists who are interested in performing research in line with goals for slowing or ending aging and human healthspan extension?

The main advice is simply to read up on the relevant experimental work that has already been done. Virtually all my conversations with scientists who initially doubt the feasibility of regenerative medicine against aging gravitate rapidly to the discovery that their pessimism arises from simply not knowing about the relevant published work. My book "Ending Aging" is a good place to start, since it is a single source for all this information with hundreds of references to the primary experimental literature.

Q. What projects is SENS working on? What lies ahead from the research?

SENS Foundation's research direction is based on two main principles: prioritise the SENS components that are not being adequately pursued through other funding sources, and prioritise those that are the most challenging. These two principles naturally overlap a lot, since difficulty is a disincentive to work on something. Accordingly, we are pursuing most of the seven SENS strands at this time. We anticipate that this will continue.

Q. How can more funding help SENS with their goals for the future?

There are no surprises there: it all about the fact that biology is irreducibly expensive. In particular, as more and more of our research programs move from the cell culture stage into live mice, the expense rises sharply.

Q. What can people look forward to in the near future from greater funding into aging research? What are a few concrete examples of near-future benefits?

I believe the main benefits we can expect to see in the coming few years will come from public health advances, and possibly from drugs to optimise metabolism. These will act, as I noted above, as a "bridge" to allow more people to survive in a healthy state for long enough to be able to benefit from the regenerative approach that SENS Foundation is pursuing.

Michael Holick on Vitamin D

Michael Holick, MD, PhD, of Boston University Medical Center says he’s “just one of the many scientists” exploring vitamin D, but he easily can be considered the world’s foremost authority on the sunshine vitamin.

In the 1970s, it was Dr. Holick who first isolated the major circulating form of vitamin D in plasma, 25-hydroxyvitamin D, as well as the active form produced by the kidneys.

He was also one of the first scientists to warn the medical community about the potential implications of widespread vitamin D insufficiency. When asked about the prevalence of low vitamin D status, he answers that it’s the “most common medical condition in the world, believe it or not.”

Dr. Holick has championed the cause of bringing vitamin D into the limelight for decades, writing numerous scientific papers as well as two popular books on the subject of vitamin D and health.

Getting D Facts from Dr. Holick

While seeking the latest findings from vitamin D research, I caught up with Dr. Holick and sought out his advice on sun exposure, vitamin D supplementation and vitamin D’s potential ties to weight management, insulin resistance and heart health.*

Q: Dr. Holick, thank you for taking the time to update us on vitamin D research. Elvis Presley once said, “Truth is like the sun. You can shut it out for a time, but it ain’t going away.” Don’t you think this quote represents the vitamin D story?

A: Amen. Elvis was right on target. Our sun has been demonized for 40 years unchallenged. It’s quite remarkable that it’s part of the psyche of the world. But it’s caused a major problem, which is worldwide vitamin D deficiency [or insufficiency] and markedly increased risk of chronic disease for children and adults.

You can instantly make vitamin D, but if you’re avoiding the sun as most people do it puts you at high-risk of deficiency. Why is that? It’s been demonized for so long because the dermatologists have come out with the big “C” word [melanoma skin cancer from sun exposure]. And there’s no question that skin cancer is on the rise. The major reason is because back in the ’60s people used to put baby oil on and bake in the sun. Right? Now, all of the sudden, that’s starting to haunt them later in life. It increased their risk of non-melanoma skin cancer.

But often what people don’t realize is that melanoma, the most deadly cancer—which is also what they lump together with skin cancer from the sun—most melanomas occur on the least sun-exposed areas. Occupational sun exposure decreases your risk of developing melanoma. There was a study done in a group in Texas that if you had the most sun exposure as a child and young adult and you did get melanoma, then you were more likely to survive it.

Q: Would you comment on vitamin D being a hormone, and the oldest hormone?

A: Well, the reason why we say that [it's the oldest hormone] is because I asked the question several years ago. If you take phytoplankton—there’s a phytoplankton species called Emiliani huxleii has been identified as one of the oldest phytoplankton species that has been unchanged for 750 million years. When we looked at that organism, it made a huge amount of vitamin D when it was exposed to sunlight.

It’s a hormone you make in your skin, then it’s inactive. It has to go to your liver to get hydroxylated to 25-hydroxyvitamin D, which is the major circulating form, the form you should ask your doctor to test for vitamin D status. Then it goes to your kidneys where it’s activated to 1,25-dihydroxyvitamin D, then it goes to your bone and intestines and kidneys.

Q: As a hormone, we also know now that it has a greater role on the body besides speeding up absorption of calcium for bone health. There is a link to cardiovascular health, right? What’s the state of the science?

A: As for the heart, we know that vascular smooth muscle cells have vitamin D receptors and we know that vitamin D seems to play a role in regulating blood pressure, regulating heart muscle cells in their growing activity, regulates to some degree the strength of the heart in terms of its pumping ability. That’s why it’s not at all surprising that just two years ago out of the Framingham heart study it shows that if you are vitamin D deficient you [are not providing optimal support for cardiovascular health].

Q: How does vitamin D’s relationship to heart health affect you if you are overweight?

A: This issue for obese people is particularly important because vitamin D is fat-soluble and is incorporated in your body fat. We showed many years ago that if you take an obese person and give him an oral dose of vitamin D or put him in a [UVB] tanning bed, it only raises his blood level to less than 50 percent than what a normal-weighted individual does and we’re talking about a BMI [Body Mass Index] of greater than 30. He needs two to three times more [of vitamin D than a person of normal BMI].

We know that obese people have more aches in their muscles, which is definitely due to vitamin D deficiency. They have muscle weakness. They’re fatigued. They just don’t want to go. It’s in part due to the deficiency. We also know that fat cells have a vitamin D receptor. There’s some evidence—we’re doing some research right now—that suggests that maybe vitamin D helps keep fat cells in check.

Q: Really? By what mechanism is it that you think vitamin D could help keep fat cells in check?

A: It may regulate fat cell maturation. It may regulate fat cell fat accumulation. That’s brand new stuff that we’re taking a look at that we’ve not yet published on. We’re just beginning to look at it.

Q: Is there any relationship established between low vitamin D status and insulin sensitivity?

A: We think so. We know that from NHANES (National Health and Nutritional Examination Survey) that [there may be a relationship associated with insulin sensitivity].

Q: We’ve heard a lot about a new established relationship between vitamin D and the immune system. Would you comment on the mechanism by which vitamin D is involved?

A: Well we know is that your immune system is regulated by vitamin D. We know that the cell macrophages definitely gobble up infectious agents because of vitamin D, macrophages activate vitamin D locally, and it stimulates production of a defensive protein that kills infectious agents. A study was done to show that if you raise your blood level, that you have more activity of your macrophages in killing infective agents. If there’s anything out there that helps to support the immune system, it’s probably vitamin D.

Q: Do you agree that everyone should be checked for vitamin D status?

A: Well, that’s the problem. It’s not an unreasonable thing to do, but I can already tell you they’re deficient. We know almost everyone’s deficient. If a normal adult isn’t taking at least 1,500 to 2,000 IU from supplement and diet—and you can’t really get it from your diet—then we know you’re vitamin D deficient. And so, to try to screen everybody, all the obese people in the United States is such a huge cost burden.

In fact, Medicare is looking at this right now and wanting to control the doctors’ use of that assay. They do not want to use it as a screening tool. I don’t disagree with that. Because we know that you can very effectively correct vitamin D deficiency, treat it, and prevent it from occurring again, if you give the person enough vitamin D. So only if they have fat malabsorption syndrome, or has had gastric bypass surgery, or cystic fibrosis, IBD, or celiac sprue—all of those individuals should be tested because you can’t predict whether or not they’re going to be able to absorb the vitamin D that you give them as a supplement.

Q: What about older people? Does the requirement for vitamin D supplementation increase with older age because of declined absorption?

A: No it does not. That’s what everybody says. [Note: Elderly can absorb vitamin D as easily as younger people.] What does change with age is the ability to make it in your skin. We showed many years ago that if you compare a 70-year-old to a 20-year-old, the 70-year-old will have about a 70 percent reduced ability to produce vitamin D. But we also went on to show that you can take an older person and still have them exposed to sunlight or simulated sunlight and they make a lot of vitamin D. Your body has a huge capacity to make vitamin D. We showed that healthy adults in bathing suits getting a minimal erythermal dose get an equivalent to ingesting 20,000 IU of vitamin D.

Now you begin to understand why the 100 IU in a glass of milk or orange juice or the 400 IU in a multivitamin is probably one tenth of what we really need to satisfy our body’s requirements for heart health or for reducing risk diseases.

Q: Do you agree as other scientists have suggested that the average person should be getting at least 20 minutes of sunshine per day for adequate vitamin D intake along with supplementation?

Dr. Holick has been researching vitamin D since the 1970s.
A: I don’t know about 20 minutes a day because it depends upon time of day, season of the year, latitude, and your degree of skin pigmentation. What I tell people is, if you know that you’re going to be out in June at noon-time for 30 minutes, in Arizona, and you’re going to get a light sunburn to your skin, to go out 50 percent of that time.

Always protect your face, it’s the most sun exposed, the most sun damaged. But you can certainly expose your arms and legs and not worry about it, in my opinion. Abdomen, back, not a problem. The more skin you expose, the more [vitamin D] that you make.

Q: Do you expect the Institute of Medicine’s recommendations for Adequate Intake of vitamin D to change in the United States anytime soon to reflect findings of new research?

A: Yes, there will definitely be new Adequate Intakes. What you really care about though is not the AI recommendation, what you care about is the Upper Limit—that’s what prevents manufacturers from putting vitamin D into foods. The amounts that you can put in and the amounts that supplements can contain.

The safe upper limit right now is considered to be 2,000 IU for adults. The major manufacturers like Coca Cola or who make Minute Maid orange juice for example put only 100 IU in a glass, because if they put in any more then they start adding that up, drinking milk and taking a multivitamin, you’re over the 2,000 IU limit.

Then if you get some toxicity like a kidney stone, it doesn’t matter that it’s not due to the vitamin D, the lawyers will say that it is if you put more than you should’ve put in. So they need to increase it like to 10,000 IU in which case, then we can really have an impact on the entire U.S. population and the world’s population because they could now put more vitamin D in the food.

Q: Dr. Holick, this has been very interesting and I’m sure it will be interesting to our readers. Thank you for your time. Also, congrats on the new book. We’ll be ordering a couple of copies for our library.

A: Wonderful. Feel free to stay in touch

Nutrition and Breast Cancer

Thanks to recent research in nutrition, dietary strategies are helping many more women survive breast cancer and go on to live long, healthy lives. 

Often enough, evidence reveals these strategies may work by influencing inflammation, the immune system, and insulin responsiveness. However, there is no nutritional therapy that is yet "proven" to treat cancer directly or increase survival.

According to large trials of diet and breast cancer such as the Women's Healthy Eating and Living (WHEL) randomized trial and the Women's Intervention Nutrition Study (WINS) trial, as well as small intervention studies, a lower calorie diet leading to controlled weight reduced mortality. 

The reason - being overweight or obese appears to increase mortality because of higher risk of metastasis. Crash dieting is not the key, only healthy weight loss and patients should consult a nutritionist for planning meals. 

Patients should note that diets too low in calories can lead to loss of muscle mass, which is already a side effect of chemotherapy, and that generally leads to an increase in fat mass. 

As far as types of foods, red meat should be avoided because it's associated with increased risk of breast cancer. Saturated fat should be avoided as much as possible since it increases estrogenic stimulation of breast cancer growth. 

A low-fat, high-fiber diet is associated with suppressed estradiol levels. The diet should be based on plenty of plant-based proteins (soy, wheat), eggs, fish and low-fat dairy (whey). 

High-carb diets are also associated with increased mortality, but so are very low-cab diets. The diet should focus on obtaining a moderate amount of complex carbs (mainly from whole grains, fruits, and vegetables) rich in fiber. Blood sugar control is encouraged through eating complex carbs and obtaining regular exercise. 

Patients should seek to obtain higher levels of long-chain omega-3 fatty acids (DHA and EPA) such as from fish oil because low levels are associated with more proinflammatory markers. 

Because high dietary intake of fruits and vegetables are associated with greater breast cancer survival, it's easy to suggest that taking supplements of phytochemicals may increase survival. However, meta-analyses suggest no single vitamin/phytochemical solely improves outcomes. Instead it's best to focus on consuming more of whole fruits and vegetables.

Phytoestrogens such as from soy (isoflavones) and flax may, in fact, lower risk of breast cancer and improve survival of breast cancer. Because they mimic estrogen and bind to estrogen receptors, they may inhibit cancer cell growth. However, more research is needed before suggesting as a treatment especially in high-risk women and postmenopausal estrogen-receptive positive breast cancer patients.  Note that it could be that simply replacing meats with soy foods leads to weight management that increases breast cancer survival.

Eating foods rich in iodine such as sea vegetables or using iodized salt may anticarcinogenic effect possibly by optimizing thyroid function. Additionally, maintaining a high vitamin D status may help reduce risk cancer and improve prognosis although more research is needed to understand the relationship.  

Reference 

Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.

10 Steps for Patients with Cholesterol-Induced Cardiomyopathy

Cardiomyopathy is characterized by a weakened, enlarged or inflamed cardiac muscle. The disease may be in primary stages (asymptomatic) or secondary stages (symptoms such as shortness of breath, fatigue, cough, orthopnea, nocturnal dyspnea or edema) with main types being dilates, hypertrophic, restrictive, or arrhythmogenic (1). Treatment may include drugs such as ACE inhibitors and beta blockers, implantable cardioverter-defibrillators, cardiac resynchronization therapy, or heart transplant (1). Factors leading to cardiomyopathy may include alcohol consumption, smoking, obesity, sedentary lifestyle, smoking and high-sodium diet (1).

Hypercholesterolemia can lead to fatty streaks in blood vessels that result in decreased flow of blood through arteries. The advent of hypercholesterolemia may be directly related to cardiomyopathy as it’s well established as a risk factor in inducing systolic and diastolic dysfunction (2). Statins such as Lovastatin are commonly prescribed because of efficacy for lowering cholesterol levels and they act by inhibiting HMG-CoA reductase to deplete mevalonate (3). Mevalonate, a precursor to cholesterol is also a precursor to coQ10 and squalene (4). Mevalonite, however, is also the precursor to coQ10 and squalene. Both of these are vital nutrients with profound effects on the body.

Patient Recommendations

I would advise a patient with cholesterol-induced cardiomyopathy to adhere to the following protocol:

1. Quit smoking – If the patient smokes, he is doing himself a grave disservice as smoking can increase oxidation of cholesterol leading to atherosclerosis. It may be an underlying factor in his cardiomyopathy.

2. Regular exercise – If the patient doesn’t exercise already, then he should begin an exercise program to strengthen his heart. I would advise only short periods of exercise combined with adequate rest as opposed to aerobic training because it would prevent exhaustion or excessive stress on the heart (9).

3. Get blood pressure checked regularly – Hypertension can be present without any symptoms and can be an etiological factor in cardiomyopathy. At ages past 60 there begins to be a higher risk of developing hypertension as well as declining muscle mass replaced by fat mass. A DASH eating plan (low-fat dairy products, lean meats, rich in fruits and vegetables) can assist in lowering or maintaining healthy blood pressure levels.

4. Lose weight if necessary – Overweight and obesity is an additional risk factor for hypertension (and hypercholesterolemia) because it increases volume of blood flowing through blood vessels. Along with exercise and a DASH eating plan, a weight-management program to lower calories steadily for 1-2 pounds per week can help a person lose weight effectively and safely.

5. Eat a diet high in soluble fiber – Diets high in soluble fiber are associated with lower levels of cholesterol. Soluble fiber such as from oats and psyllium hulls are shown to reduce blood cholesterol by inhibiting absorption of cholesterol from food as well as reabsorption of cholesterol through enterohepatic circulation.

6. Supplement with coQ10 (100 mg) – CoQ10 production peaks in the mid-20s and begins to decline with only around 50 percent production in patients past age 60. Additionally, statin therapy creates further decline in coQ10 synthesis for reasons discussed above. This patient could benefit from regular daily coQ10 supplementation in 100 mg doses. The CoQ10 will serve to support creation of energy and mitochondrial biogenesis in cardiac tissue to help maintain strong heart function.

7. Enjoy enough sunshine and take a vitamin D supplement – As people become older they are more susceptible to vitamin D insufficiency or deficiency, which as discussed earlier may lead to a weakened heart as suggested by emerging studies. Support for heart health can be achieved by keeping 25(OH)D to levels in the plasma to “sufficient” amounts (32 ng/mL) through sensible sun exposure (maybe along with exercise) and/or supplementation with vitamin D.

8. Supplement with D-ribose and l-carnitine – Both supplements can support elevated energy levels in cardiac tissue leading to improved heart function. In a randomized, double-blind crossover trial, D-ribose has been shown to improve diastolic function parameters and improve quality of life in patients with cardiomyopathy (10). L-carnitine combined with coQ10 and omega-3 fatty acids has been shown to improve cardiac function in dilated cardiomyopathy (11).

9. Eat leafy greens – Apart from the extra dietary fiber, the magnesium in leafy greens can be an additional support for heart health. Magnesium has a role in supporting healthy blood pressure levels and regulating heart function (12).

10. Eat fish regularly or take a quality fish oil supplement (4g daily) – Greater levels of EPA and DHA omega-3 fatty acids in the diet combined with coQ10 and l-carnitine has been shown in research to improve cardiac function in dilated cardiomyopathy (11).

Reference List

1. Wexler RK, Elton T, Pleister A, Feldman D. Cardiomyopathy: an overview. Am Fam Physician 2009;79:778-84.

2. Huang Y, Walker KE, Hanley F, Narula J, Houser SR, Tulenko TN. Cardiac systolic and diastolic dysfunction after a cholesterol-rich diet. Circulation 2004;109:97-102.

3. Littarru GP, Langsjoen P. Coenzyme Q10 and statins: biochemical and clinical implications. Mitochondrion 2007;7 Suppl:S168-S174.

4. Scharnagl H, Marz W. New lipid-lowering agents acting on LDL receptors. Curr Top Med Chem 2005;5:233-42.

5. Jeya M, Moon HJ, Lee JL, Kim IW, Lee JK. Current state of coenzyme Q(10) production and its applications. Appl Microbiol Biotechnol 2010;85:1653-63.

6. Caso G, Kelly P, McNurlan MA, Lawson WE. Effect of coenzyme q10 on myopathic symptoms in patients treated with statins. Am J Cardiol 2007;99:1409-12.

7. Visvanathan R, Chapman I. Preventing sarcopaenia in older people. Maturitas 2010.

8. Ahmed W, Khan N, Glueck CJ et al. Low serum 25 (OH) vitamin D levels (<32 ng/mL) are associated with reversible myositis-myalgia in statin-treated patients. Transl Res 2009;153:11-6.

9. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.

10. Omran H, Illien S, MacCarter D, St Cyr J, Luderitz B. D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study. Eur J Heart Fail 2003;5:615-9.

11. Vargiu R, Littarru GP, Faa G, Mancinelli R. Positive inotropic effect of coenzyme Q10, omega-3 fatty acids and propionyl-L-carnitine on papillary muscle force-frequency responses of BIO TO-2 cardiomyopathic Syrian hamsters. Biofactors 2008;32:135-44.

12. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

Low muscle mass linked to diabetes

Being overweight is a risk factor for type 2 diabetes; however, a new study shows losing weight alone may not be enough to reduce risk of type 2 diabetes in people with low muscle mass and strength, particularly if they are over the age of 60.

These are the findings of new research from Dr. Preethi Srikanthan of University of California, Los Angeles, and colleagues who performed a cross-sectional analysis of 14,528 people from National Health and Nutrition Examination Survey III.

Dr. Srikanthan and colleagues concluded that age-related muscle loss, or sarcopenia, was associated with greater insulin resistance; and, sarcopenia, independent of obesity, may be an early predictor of diabetes. This association of sarcopenia and insulin resistance was strongest in those who were 60 years and older, the researchers warn.

Apart from these poor health outcomes, sarcopenia in older adults is also clearly associated with other health outcomes such as increased risk of falls, hip fractures, bone loss (osteopenia) and physical disability.
Several earlier studies suggest similarly that a direct correlation exists between sarcopenia in people ages 60 and older and greater risk of insulin resistance, metabolic syndrome, type 2 diabetes and cardiovascular disease, regardless of body weight.

Study Reference: Srikanthan P, Hevener AL, Karlamangla AS, 2010 Sarcopenia Exacerbates Obesity-Associated Insulin Resistance and Dysglycemia: Findings from the National Health and Nutrition Examination Survey III. PLoS ONE 5(5): e10805. doi:10.1371/journal.pone.0010805

Briefly on Detoxification Systems

Every day we are exposed to toxins, or xenobiotics, that are found in our food, water and environment. The body also makes toxins within itself. These all must be either stored such as in muscle or fat or they are  detoxified and eliminated via the feces or urine.

The body's main detoxification organ is the liver, but can also happen in the intestine and other organs. The detoxification systems handle a wide range of compounds mainly by two steps: phase I and phase II detoxification. 

Phase I detoxification is a reaction that entails functionalization of the compound, breaking it down. The major P450 enzymes are generally involved in phase I detoxification. Most major drugs and exogenous toxins are metabolized this way. At times the product of phase I detoxification can be more harmful than the original product.  

Phase II detoxification is a second reaction that generally follows phase I detoxification. It entails transforming a phase I reactant through conjugation (typically to an amino acid, such as in glucuronidation or sulfation) to become water soluble. When it's water-soluble, the toxin can be excreted in the urine. 

Although the phases of detoxification are not yet well understood, it is clear through observational studies that there are a variety of factors that can inhibit or induce detoxification. An inducer of detoxification can be a a toxin itself or a compound in the diet. 

In a typical detoxification support plan, a nutritionist may suggest various nutrients to support or upregulate phase I cytochrome P450 enzymes and phase II conjugation pathways. 

The plan would generally seek to increase glutathione levels in the body such as with n-acetyl cysteine or cysteine or spare glutathione such as with silymarin. 

The plan may also support detoxification in other ways by increasing antioxidant status with coenzyme Q10, vitamin A, vitamin C, or selenium. Or, it may provide B vitamins to act as co-factors for enzymes.  

Reference

http://www.thorne.com/altmedrev/.fulltext/3/3/187.pdf 

62-yr-old Woman with Hypertention, Ventricular Hypertrophy and Congestive Heart Failure

One of the considerations with congestive heart failure is the need for fluid restriction and the patient will need to work her doctor to be able understand how much she should be getting daily.

Sodium restriction is important for bringing down the blood pressure. In the case of this woman, I would employ a DASH diet to bring down her blood pressure with emphasis on plenty of fruits and vegetables as well as dairy products such as yogurt to obtain regular amounts of calcium.
Since being overweight contributes to higher blood pressure, if she is overweight, then the DASH diet should be combined with a weight loss program by restriction of calories.

Regular aerobic exercise can also support healthy blood pressure levels. I'd recommend about 30 minutes three times weekly.

Because of her condition, I'd also recommend supplementation with CoQ10 to support the function of the heart. If she has a low vitamin D status, which is associated with higher blood pressure, then I'd also recommend a vitamin D supplement.

Gallstone Development

Gallstones develop in the gallbladder, a small organ that stores and releases the bile made by the liver. Bile is a dark green fluid containing bile salts and cholesterol. The gallbladder releases bile into the small intestine to assist in digesting fats more efficiently. However, if the bile is contains high concentrations of cholesterol, then stones too difficult for the bile salts to dissolve may develop (1).
Losing weight too quickly or fasting can cause development of gallstones. The quick weight loss and fasting is thought to disturb the balance of bile salts and cholesterol (2;3).

The risk may increase if consuming a diet too low in fat. Avoiding fat reduces frequency of gallbladder emptying. This, in turn, may cause cholesterol to accumulate and lead to greater risk of forming stones (3;4).

References

1. Dowling RH. Review: pathogenesis of gallstones. Aliment Pharmacol Ther 2000;14 Suppl 2:39-47.

2. Wudel LJ, Jr., Wright JK, Debelak JP, Allos TM, Shyr Y, Chapman WC. Prevention of gallstone formation in morbidly obese patients undergoing rapid weight loss: results of a randomized controlled pilot study. J Surg Res 2002;102:50-6.

3. Festi D, Colecchia A, Orsini M et al. Gallbladder motility and gallstone formation in obese patients following very low calorie diets. Use it (fat) to lose it (well). Int J Obes Relat Metab Disord 1998;22:592-600.

4. Vezina WC, Grace DM, Hutton LC et al. Similarity in gallstone formation from 900 kcal/day diets containing 16 g vs 30 g of daily fat: evidence that fat restriction is not the main culprit of cholelithiasis during rapid weight reduction. Dig Dis Sci 1998;43:554-61.

Homocysteinemia and Pernicious anemia

Pernicious anemia, a megaloblastic anemia caused by B12 deficiency, is associated with hyperhomocysteinemia. Because B12 is needed for methionine synthase to methylate homocysteine to methionine, a deficiency causes an accumulation of both homocysteine and methylmalonic acid (1). When both are elevated, marking the pernicious anemia, it can lead to progressive demyelination and neurological deterioration.
A folate deficiency may also result in megaloblastic anemia. If homocysteine is elevated but not methylmalonic acid, then the result is probably a folate deficiency. It is important for treatment to be correct. Large doses of folate can correct, or "mask," symptoms of pernicious anemia, which can result in irreversible neuropathy (2).
References

1. Devlin TM. Textbook of Biochemistry with Clinical Correlations. Philadelphia: Wiley-Liss, 2002

2. Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006

Before Taking a Statin, Read This

I thought this was an interesting article from Businessweek a couple of years ago and was blown away by the numbers showing that few people actually receive any benefit from statins.

If you don't read it, then here are a few tidbits from the article that I thought would give it to you in a nutshell:

• ...for every 100 people in the trial, which lasted 3 1/3 years, three people on placebos and two people on Lipitor had heart attacks. The difference credited to the drug? One fewer heart attack per 100 people. So to spare one person a heart attack, 100 people had to take Lipitor for more than three years. The other 99 got no measurable benefit.
• ...an estimated 10% to 15% of statin users suffer side effects, including muscle pain, cognitive impairments, and sexual dysfunction
• "There's a tendency to assume drugs work really well, but people would be surprised by the actual magnitude of the benefits,"
• For anyone worried about heart disease, the first step should always be a better diet and increased physical activity. Do that, and "we would cut the number of people at risk so dramatically" that far fewer drugs would be needed...
• "The way our health-care system runs, it is not based on data, it is based on what makes money."  

It's amazing how much industry and their marketing overstate claims and directly affect the beliefs of people in these drugs. This kind of influence in our healthcare system desperately needs to be fixed.

Predicting a Heart Attack with CRP

Currently, the existing biomarkers for a cardiac event include B-type natriuretic peptide, tro-ponins and C-reactive protein. C-reactive protein is an acute-phase protein released in response to inflammation.

Recently, the development of a high-sensitivity assay for CRP (hs-CRP) has been made available. The assay works because it can accurately reflect even low levels of CRP. There have been quite a few prospective studies that have shown that an assay of a baseline CRP can be used as a marker for cardiovascular events.

When patients have a test that shows elevated levels, it is even a better marker than LDL cholesterol for predicting events such as myocardial infarction. An elevated test, however, can also mean hypertension, metabolic syndrome or diabetes, or a chronic infection.

In addition, Lipoprotein (a), or Lp(a), when combined with C-reactive protein, can increase the predictive value of a cardiac event. This is especially true for those who have normal cholesterol levels. The reason is that the lipoprotein promotes vascular inflammation that affects the atherogenic process directly.

Reference

Pagana, K.D., Pagana, T.J. Mosby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006.

How to Rid Yourself of Statin-induced Muscle Pain

When a patient is on a statin, nutritionists should advise that they don’t have to suffer from the side effects of statin-associated muscle pain (myalgia). Studies are showing that supplementation with two key compounds are useful for decreasing the pain. The first is ubiquinone (coenzyme Q10, coQ10) and the other is cholecalciferol (vitamin D3).

Statins such as Lipitor, Zocor and Mevacor reduce cholesterol synthesis by directly inhibiting the enzyme HMG-CoA reductase and deplete production of its product, mevalonate (1). Mevalonite, however, is also the precursor to coQ10 and squalene. Both of these are vital nutrients with profound effects on the body.

CoQ10

CoQ10 is a lipid-soluble antioxidant playing a protective effect in the membranes of every cell in the body. In that capacity, it serves to protect against oxidative damage to cells. Equally important, the compound is necessary for electron transfer in the mitochondrial electron transport chain for producing energy (2). Without it, our muscles could not function in their full capacity.
Supplementation with coQ10 combined with statin treatment helps reduce muscle pain (not to mention improve energy levels). According to a double-blind study in 2007 at Stony Brook University, which compared coQ10 supplementation (100mg/d) with vitamin E (400 IU/d), showed that patients taking the coQ10 had 40 percent decrease in the severity of their pain (3).

Vitamin D

Squalene is important because it is the precursor for 25 hydroxyvitamin D (25(OH)D) as well as other steroid hormones. For this reason that, it is suggested that statin drugs can lead to 25(OH)D insufficiency or deficiency. Vitamin D is not only critical for speeding up calcium absorption for bone health, but emerging studies are finding that it’s also vital for the health of muscles (4).
Low vitamin D levels are also associated with statin-induced muscle pain. When researchers from the Cholesterol Center at the Jewish Hospital in Cincinnatti in Ohio treated myalgia in 38 statin-treated patients with vitamin D (50,000 IU/week for 12 weeks), 35 of the patients experienced 92 percent reduction in pain symptoms (5).

Reducing muscle pain with supplementation

If you must take a statin, then supplementation can be to your advantage. As in the studies, supplementation with coQ10 at 100 mg in an absorbable form can potentially help to keep pain under control by replenishing coQ10 that is lost. In addition, keeping 25(OH)D to levels in the plasma to “sufficient” amounts (32 ng/mL) through supplementation with vitamin D and sensible sun exposure can go far to reduce pain.

Reference List

1. Scharnagl H, Marz W. New lipid-lowering agents acting on LDL receptors. Curr Top Med Chem 2005;5:233-42.
2. Jeya M, Moon HJ, Lee JL, Kim IW, Lee JK. Current state of coenzyme Q(10) production and its applications. Appl Microbiol Biotechnol 2010;85:1653-63.
3. Caso G, Kelly P, McNurlan MA, Lawson WE. Effect of coenzyme q10 on myopathic symptoms in patients treated with statins. Am J Cardiol 2007;99:1409-12.
4. Visvanathan R, Chapman I. Preventing sarcopaenia in older people. Maturitas 2010.
5. Ahmed W, Khan N, Glueck CJ et al. Low serum 25 (OH) vitamin D levels (<32 ng/mL) are associated with reversible myositis-myalgia in statin-treated patients. Transl Res 2009;153:11-6.

How a Patient May Avoid An Angioplasty

Angioplasty is a procedure performed by inserting a catheter with a deflated balloon into an affected artery, then inflated to open the artery. Sometimes a stent, or mesh tube, is left to keep it open. The procedure does come with some risk, in fact, having the potential of inducing a heart attack.

If a patient is uncomfortable with an angioplasty, there are now other alternatives that may be just as effective without the procedure.

Medical researchers, for example, have been evaluating the combined approach using anti-coagulants, thrombolytic therapy (clot-dissolving drugs) and cholesterol-lowering drugs. According to Dr. Eric J. Topol of the Cleveland Clinic, the treatment has been deemed effective in at least a few small studies (1).

Other cardiologists look to intensive-lipid therapy alongside dietary supplements such as fish oil and vitamin D. According to Dr. William Davis, the integrated therapy has been shown to help slow progression of atherosclerosis and even reverse it in asymptomatic adults (2).

Along with treatment, the patient should adopt exercise and special dietary considerations to help provide a complete comprehensive treatment of risk factors including control of hypertension, obesity and type 2 diabetes (3). For this patient, diet should be low in saturated and trans fat, high in fiber, and provide optimal levels of nutrients such as omega-3 fatty acids, and vitamin D for lowering cardiovascular risk (3).

A DASH eating plan can help to meet diet goals. The eating plan, which has been found to lower blood pressure within 15 days, features low-fat dairy products, fish, and lean meats as well as plenty of whole grains, fruits and vegetables. Recently, a study found that a DASH eating plan combined with exercise helped subjects to reduce blood pressure, lose weight, improve mental function, and improve cardiovascular fitness (4).

References

1. Topol EJ. Integration of anticoagulation, thrombolysis and coronary angioplasty for unstable angina pectoris. Am J Cardiol. 1991 Sep 3;68(7):136B-141B.
2. Davis W, Rockway S, Kwasny M. Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults. Am J Ther. 2009 Jul-Aug;16(4):326-32. Available at: http://www.ncbi.nlm.nih.gov/pubmed/19092644
3. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
4. Smith PJ, Blumenthal JA, Babyak MA, Craighead L, Welsh-Bohmer KA, Browndyke JN, Strauman TA, Sherwood A. Effects of the Dietary Approaches to Stop Hypertension Diet, Exercise, and Caloric Restriction on Neurocognition in Overweight Adults With High Blood Pressure. Hypertension. 2010 Mar 19. [Epub ahead of print]

Atherosclerosis

Atherosclerosis refers to accumulation of a thick sludge in patches that merge to form large plaques, called atheromas, in artery walls. The plaque is made up of cholesterol and other fats, macrophages, cell "junk", calcium, and tissues.

LDL cholesterol is associated with atherogenesis because as it becomes oxidized it can induce endothelial cells to attract blood-borne monycytes, transforming them into macrophages and trapping them in endothelial spaces (1).

The macrophages then engorge themselves with cholesterol and fat creating "foam cells. Then, once engorged, they release inflammatory cytokines that only lead to even more macrophages creating more foam cells (1).

Along with damaged smooth muscle cells, the foam cells then form the sludge plaque, or fatty streak, that narrows lumen as it grows larger causing blood flow to to become restricted (1).

Medications

There are various drugs that can help to slow or reverse atherosclerosis, which include cholesterol-lowering drugs such as statins, anti-coagulants such as warfarin to inhibit clotting, antiplatelets like aspirin to keep platelets from forming clots, and medications such as ACE inhibitors or calcium channel blockers to lower blood pressure (2).

If atherosclerosis becomes severe, surgery may be needed. A procedure called an angioplasty can be performed by inserting a catheter with a deflated balloon into an affected artery, then inflated to open the artery. Sometimes a stent, or mesh tube, is left to keep it open.

Other surgeries involve endarterectomy, where fatty deposits are surgically removed from walls, or thrombolytic therapy in which drugs are inserted into arteries to dissolve clots (2).

A bypass surgery (such as a CABG, coronary artery bypass surgery) involves using another part of the body or a tube to allow blood to flow around an affected artery (2).

Lifestyle changes

It is possible to change the course of atherosclerosis -- even possibly reverse it -- by adopting a few lifestyle changes. These include stopping smoking, exercising regularly, eating right and lowering stress.

- Smoking in itself oxidizes LDL cholesterol and hastens the damage of arteries.
- Exercise improves blood flow and can induce the development of new blood vessels to lower the pressure on affected arteries.
- Eating right should include adopting strategies such as managing portions for weight management, a DASH-style diet for lowering blood pressure, limiting saturated and trans fatty acids and adopting polyunsaturated fats to lower triglycerides, and eating a high-fiber diet to lower cholesterol levels (1).
- Limiting stress in life through relaxation and sleeping well helps to avoid rises in blood pressure.

Overall, it's very likely that almost half of us will die from atherosclerosis or complications relating to it. Almost all of us have fatty streaks and plaques already developing. These are disheartening figures for those of us who wish to do all we can to fight back.

Luckily, our nutrition and medical knowledge continues to improve and new technologies are also forming.

One program of interest is the one promoted by cardiologist Dr. William Davis in his book Track Your Plaque, who promotes actively "tracking" the progression of plaque development (3).

In addition, Dr. Davis and fellow scientists have studied the effects of combined therapies involving niacin or statins, fish oil, vitamin D and other means to slow or reverse "hardening of the arteries" (4).

Reference List


1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. http://www.mayoclinic.com/health/arteriosclerosis-atherosclerosis/DS00525/DSECTION=treatments%2Dand%2Ddrugs
3. http://www.trackyourplaque.com
4. Davis W, Rockway S, Kwasny M. Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults. Am J Ther. 2009 Jul-Aug;16(4):326-32. Available at: http://www.ncbi.nlm.nih.gov/pubmed/19092644

Sodium: How much is right for you?

Sodium’s association with high blood pressure is well known. However, sodium also plays a large role in keeping you healthy. It’s important to know how to strike the right balance.

Along with potassium, sodium is essential for fluid balance, facilitating the flow of water in and out of cells to bring nutrients in and take wastes away. Sodium also has a role in the regulation of blood pressure and helping muscles and the heart relax. Each sodium ion contains an electrical charge, acting as an electrolyte, which allows transmission of nerve impulses to the brain and throughout the body.

Sodium levels in the body are controlled by the kidneys. If the body doesn’t receive enough sodium daily—a chronic problem for our early ancestors—then the kidneys retain sodium. When the body has a high enough amount, then the excess sodium is excreted in the urine.

At times, sodium levels may fluctuate. If a person has a dysfunctional kidney, then the body may retain too much sodium, which can result in edema, or swelling in the legs and feet because sodium attracts water. In contrast, diarrhea or vomiting may result decreased sodium levels, a condition known as hyponatremia.

How sodium regulates blood pressure is not entirely understood, but there is an established link between high sodium intake and high blood pressure. As expected, there is also a link between sodium reduction and lower blood pressure.

The sodium-hypertension relationship may also have to do with how sodium interplays with other minerals such as potassium and calcium. Potassium, for example, appears to assist the kidneys in shedding excess sodium. Lowering sodium intake also helps to conserve calcium, which may affect blood pressure.

Recommendations for Sodium

The Institute of Medicine is recommending an Adequate Intake of sodium at 1,500 mg per day for adults and children 9-13 as well as 1,000 mg and 1,200 mg per day for children ages 1-3 and 4-8, respectively. These levels are considered appropriate for replacing daily losses via sweat and urine. The need for sodium may be slightly greater if exercise produces excessive sweating or if a person has symptoms of vomiting or diarrhea.

On average, however, most adults in the U.S. consume about 3,200 milligrams or more a day. With these figures, it is easy to understand why high blood pressure affects nearly 75 million Americans. The average intake is well above the Institute of Medicine’s Tolerable Upper Intake Level of 2,300 milligrams per day for adults and 1,500mg, 1,900mg and 2,200 mg for children ages 1-3, 4-8 and 9-13, respectively.

Cutting sodium intake daily tor recommended levels is important and it doesn’t have to be difficult with these three simple strategies:

Sodium Strategy #1: Limit processed or prepared foods high in sodium. Most sodium in the diet doesn’t come from the salt shaker, but from processed and prepared foods. Thus, the best way to lower sodium is to reduce intake of processed foods or replace them with low-sodium alternatives. This includes ready-to-eat packaged foods such as potato chips, fast-food meals such as burritos, and highly salted meals prepared at restaurants.

Sodium Strategy #2: Learn to enjoy food without salt. Taste food before salting it; the food may already be salty enough or it may be enjoyed without salt. In fact, salty is an acquired taste. The body and taste buds can easily adjust to less salt. Studies have shown that as people reduce salt intake and stick to a relatively lower intake of sodium, they will naturally begin to prefer foods with less salt. When eating at home, try not having the salt shaker on the table and, if eating out, simply move salt shakers to another table. When preparing food, try using less salt and seasoning food with spices or salt-substitutes instead. Keep an eye on store-bought spice blends, though, as many may contain high amounts of salt.

Sodium Strategy #3: Balance sodium with potassium-rich fruits and vegetables. A clear association exists between higher potassium intake from fruits and vegetables and lower blood pressure regardless of sodium intake. Potassium helps the kidneys in promoting sodium excretion, reduces urinary calcium and magnesium (which influence blood pressure), supports smooth vascular muscle health, and helps with regulation of blood pressure.

Less Sodium in a DASH

Most people who are interested in maintaining healthy blood pressure levels would do best to follow a DASH (Dietary Approaches to Stop Hypertension)eating plan. In the well-known DASH-sodium study, which was conducted by the National Heart, Lung and Blood Institute, people following the diet lowered blood pressure in just 14 days even without reducing salt intake.

The DASH eating plan includes consuming a diet rich in low-fat, low-sodium dairy products, fish, chicken and lean meats as well as large amount of whole grains, fruits and vegetables.

When a person is concerned about blood pressure, the best advice nutritionists can give is to begin following a DASH eating plan combined with regular exercise and weight management. In fact, according to a recent study in Hypertension, this plan helped people reduce blood pressure, lose weight, improve mental function, and improve cardiovascular health.

Taking the Pressure Off of Sodium

It’s extremely easy to place all of the blame for society’s high blood pressure woes and medical costs on sodium, but the mineral’s role in the body should not be ignored. Sodium is essential for good health and too little could lead to other health issues, including deficiencies in iodine, which is mainly provided in the North American diet from iodized salt.

While lowering sodium consumption can lead to a natural preference for foods with less salt, it’s important not to cut salt out completely. Because the body requires some sodium to function properly, avoiding salt entirely might backfire, and cause cravings for high-sodium foods. As with almost all vitamins and minerals, the key to healthy sodium intake is always balance with other nutrients. A DASH eating plan and strategies for maintaining a healthy intake (such as those given above) can help you achieve this balance of nutrients for healthy blood pressure levels and optimal health.

Reference

Dyuff RL, American Dietitic Association. American Dietetic Association Complete Food and Nutrition Guide, 3rd edition. 2006. Wiley.

More reason to love olive oil

I use one particular olive oil for cooking and another extra-virgin olive oil to mix with some balsamic vinegar for my salads. Olive oil, as the staple source of fatty acids in the Mediterranean diet, has also been heavily researched for its health benefits especially in comparison to other sources of fat such as butter, corn or soy oil.

On April 20, a study in BMC Genomics was published that found that olive oil eaten at breakfast modified gene expression in patients with metabolic syndrome (1). The breakfast caused the changes in mononuclear cells after intake of the olive oil and repressed pro-inflammatory genes (1).

The study was performed on 20 patients in a double-blind randomized trial (1). The researchers noted that many of the genes were also implicated in type 2 diabetes, dyslipidemia and obesity (1).

The study adds to evidence that olive oil helps reduce inflammation unlike other oils such as butter (2) and, thereby, adds to the reasons why the Mediterranean diet is associated with lower risk of cardiovascular disease (3).

References

1. Camargo A, Ruano J, Fernandez JM, Parnell LD, Jimenez A, Santos-Gonzalez M, Marin C, Perez-Martinez P, Uceda M, Lopez-Miranda J, Perez-Jimenez F. Gene expression changes in mononuclear cells from patients with metabolic syndrome after acute intake of phenol-rich virgin olive oil. BMC Genomics. 2010 Apr 20;11(1):253. [Epub ahead of print]

2. Bellido C, López-Miranda J, Blanco-Colio LM, Pérez-Martínez P, Muriana FJ, Martín-Ventura JL, Marín C, Gómez P, Fuentes F, Egido J, Pérez-Jiménez F. Butter and walnuts, but not olive oil, elicit postprandial activation of nuclear transcription factor kappaB in peripheral blood mononuclear cells from healthy men.Am J Clin Nutr. 2004 Dec;80(6):1487-91.

3. Bellido C. Perez-Jimenez F, Alvarez de Cienfuegos G, Badimon L, Barja G, Battino M, Blanco A, Bonanome A, Colomer R, Corella-Piquer D, Covas I, Chamorro-Quiros J, Escrich E, Gaforio JJ, Garcia Luna PP, Hidalgo L, Kafatos A, Kris-Etherton PM, Lairon D, Lamuela-Raventos R, Lopez-Miranda J, Lopez-Segura F, Martinez-Gonzalez MA, Mata P, Mataix J, Ordovas J, Osada J, Pacheco-Reyes R, Perucho M, Pineda-Priego M, Quiles JL, Ramirez-Tortosa MC, Ruiz-Gutierrez V, Sanchez-Rovira P, Solfrizzi V, Soriguer-Escofet F, de la Torre-Fornell R, Trichopoulos A, Villalba-Montoro JM, Villar-Ortiz JR, Visioli F. International conference on the healthy effect of virgin olive oil. Eur J Clin Invest. 2005 Jul;35(7):421-4.


David

Fibromyalgia

Fibromyalgia, or chronic fatigue syndrome, has increased by 200 to 400 percent in the last decade and now affects approximately 6-12 million Americans. It's a syndrome with symptoms of hormonal, sleep and autonomic control dysfunctions.

Those with fibromyalgia often suffer from widespread pain in muscles, poor sleep, and low energy levels. Co-existing conditions are food reactivities and irritable bowel syndrome, migraine headaches, chronic sinusitis, restless leg syndrome and sleep apnea.

Medical treatment may include analgesics for pain relief such as with acetaminophen or NSAIDS. Most will require treatment for hypothyroidism with Armour Thyroid. A Cortef prescription or supplementation with adrenal glandulars or licorice is also helpful for adrenal support. Lastly, sex hormone therapy may be needed.

Nutritional support may include supplements of iron to guard against iron-deficiency anemia,which may contribute to lacking energy, as well as coQ10, which is fat-soluble antioxidant needed in the mitochondria for production of energy. In addition, acetyl-l-carnitine may be helpful for supporting mitochondrial energy and d-ribose may help increase energy and reduce pain.
Reference
1. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.

Preventing Lung Cancer

My dear second cousin died of lung cancer last night at midnight. This is a horrible disease and it strikes so quickly. The cancer metasticized and reached his lymph nodes and then I think he and we all knew. It's a sad day for our family. It happened so fast and it pains me that I couldn't have been with him when he passed.

Of course, as a nutritionist, my thoughts turn to what could have been done to prevent this awful day from happening. As you look through the scientific literature, of course, you end up figuring that quitting smoking is key to guarding against risk. I know my cousin had quit, but perhaps it was too late.

The only other way to help prevent this disease is simply to be sure to eat plenty of fruits and vegetables daily. The high amounts of phytonutrients probably either help to upregulate antioxidant enzymes protecting cells or act simply act as antioxidants to cells. The result is less potential damage to cell DNA.

Maybe, however, skip out on the veggies high in beta-carotene because of association with higher risk of lung cancer (the beta-carotene apparently can bind to carcinogens in smoke and potentially increase damage to DNA). That's according to the famous CARET study from Finland where beta-carotene supplements appeared to increase risk of lung cancer in smokers and those with exposure to asbestos.

I'm going to add at my cousin might have been a lot better off without all the stress. He had a high amount of stress in his lifestyle. The stress itself, science is beginning to show, leads to more oxidative stress on cells. Perhaps the constant fight-or-flight response does add stress biochemically, but it should be immediately obvious that stress in our lives leads us to eat poorly, eat less fruits and vegetables, and have have poor habits like smoking.

We all could benefit from less stress in our lives. And it leads me to pause and think, I need some good stress-management techniques. Ones that I choose such as nature walking weekly may not be enough. Sooner rather than later I need to begin a steady exercise program, eating regularly, maybe delegating some projects.

Just some thoughts.

Sent from my iPad