Marc Joseph Nutrition - Blog

At the recent “Diet and Optimum Health” conference sponsored by the Linus Pauling Institute (LPI) at Oregon State University, scientists presented research discussing some of the underlying mechanisms behind lipoic acid’s many beneficial effects.

“The evidence suggests that lipoic acid is actually a low-level stressor that turns on the basic cellular defenses of the body, including some of those that naturally decline with age,” said Tory Hagen, an LPI researcher and associate professor of biochemistry and biophysics at OSU. “In particular, it tends to restore levels of glutathione, a protective antioxidant and detoxification compound, to those of a young animal. It also acts as a strong anti-inflammatory agent, which is relevant to many degenerative diseases.” …

… “Our studies have shown that mice supplemented with lipoic acid have a cognitive ability, behavior, and genetic expression of almost 100 detoxification and antioxidant genes that are comparable to that of young animals,” Hagen said. “They aren’t just living longer, they are living better — and that’s the goal we’re after.”

Sound promising? Sure.

But there are a few things you should know about lipoic acid before running out and buying it. In fact, without a proper dosing protocol, some people may want to avoid supplementing with it entirely.

What is Lipoic Acid

Lipoic acid is a compound that contains two sulfur, or thiol, groups. The oxidized form is referred to as lipoic acid (LA), while the reduced form is called dihydrolipoic acid (DHPLA).

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There’s an interesting interview (A Longer, Better Life) in the NY Times Magazine with two medical scientists (Lenny Guarente, Ph.D., M.I.T. biology professor and researcher, and Robert N. Butler, M.D., director of the International Longevity Center) discussing the topic of aging and longevity.

Here’s a quick look at some of the opinions expressed in the interview, some of which make sense, others of which are less likely to yield results.

Quality vs. Longevity

Guarente states that his goal is improving the health and quality of life, not so much its length:

The research that I’m involved in is not about extending life after people are infirm. I don’t think of life span as the gold standard. The gold standard is health span. All the indicators from the laboratory are that the genes we’re studying and the kinds of drugs we would be developing would extend health span. If you can extend health span, and you also happen to extend life span, so be it. That’s a side benefit.

For now, I’d have to agree with that goal. Lengthening the number of high-quality health years needs to be the primary objective. That’s not to say longevity shouldn’t also be a goal, but a practical first step seems to be improving the quality of the years humans generally live, so as to reduce both the individual suffering and financial costs often associated with the final years of life.

Why Not Longevity Science?

Butler notes that as a society we haven’t really devoted the necessary resources to examining the issues of healthy aging and longevity:

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“We just fall apart,” Felix Silverstone, former senior geriatrician at New York’s Parker Jewish Institute, declares in an interesting New Yorker article on aging that’s definitely worth a read.

Aging is something we’ll all have to deal with sooner or later, whether with helping our parents or ourselves, and the article raises many of the key issues worth considering.

Why We Age

First up is the contentious question of why we age:

[S]cientists do not believe that our life spans are actually programmed into us. After all, for most of our hundred-thousand-year existence—all but the past couple of hundred years—the average life span of human beings has been thirty years or less … Today, the average life span in developed countries is almost eighty years …

… Inheritance has surprisingly little influence on longevity. James Vaupel, of the Max Planck Institute for Demographic Research, in Rostock, Germany, notes that only six per cent of how long you’ll live, compared with the average, is explained by your parents’ longevity; by contrast, up to ninety per cent of how tall you are, compared with the average, is explained by your parents’ height. Even genetically identical twins vary widely in life span: the typical gap is more than fifteen years.

The “wear and tear” model appears much more likely to determine longevity:

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Fidelity Investments just put out a report showing that a 65-year old couple retiring in 2007, with no employer sponsored coverage and a life expectancy of 85 years (women) and 82 years (men), will need $215,000 to cover health care expenses over the rest of their lives. That’s up 7 percent from last year.

The primary reasons cited for the cost increase are familiar ones:

• Demographics - more older people living longer
• Greater use of expensive medical technologies and drugs

The breakdown of the $215,000 estimate is:

• 32% for Medicare coverage premiums for expenses from doctors’ visits, outpatient hospital care and prescription drugs
• 35% for cost-sharing provisions of Medicare, including co-payments and deductibles
• 33% for out-of-pocket prescription drug costs

And, the estimate doesn’t even include:

• Over-the-counter (OTC) drugs
• Dental services
• And most importantly, long-term care

Fidelity forecasts that 50% of pre-tax Social Security benefits will be consumed by health care costs within the next 16 to 18 years.

Not Retiring Anytime Soon?

Remember, that $215,000 estimate for health care costs in retirement is for a couple retiring in 2007. At a 7% annual rate of increase, that estimate will double to over $425,000 ten years from now.

If you haven’t yet seen the 60 Minutes piece linked in this post discussing Medicare and the financial future of this country:

Why Everyone - Both Young and Old - Should Care Now About the Big Changes Coming to Medicare

it’s definitely worth checking out. There is no bigger domestic issue facing us (and most industrialized countries).

Good nutrition is the key to staying healthy and avoiding the expensive chronic conditions that account for the vast majority of health care costs. Fortunately, it’s a factor you can control. Those people who take preventive action now will definitely be in better shape, both physically and financially, as the changes in the health care system unfold.

(Image: Sheffield Estate Planning)

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Discover How Nutrition Can Make a Difference in Your Life …

Marc Joseph Nutrition

There’s quite a bit of research that suggests calorie restriction (CR), as long as essential nutrient needs are met, may help to significantly reduce disease risk and improve longevity. There are even organizations focused solely on the topic.

Researchers at the University of California and Children’s Hospital Oakland Research Institute note in a paper in the 2007 Annual Review of Nutrition that even reducing calorie intake later in life may lead to beneficial effects (e.g., preventing or slowing the growth of cancer).

The article mentioning the paper discusses some of the possible ways CR may work:

Physiological changes associated with aging include cell damage and the emergence of cancer cells. The most important effects of low calorie diets and longevity therapeutics given late in life may not be to prevent this damage, but instead to stimulate the body to eliminate damaged cells that may become cancerous, and to stimulate repair in damaged cells like neurons and heart cells. Low calorie diets drive the body to replace and repair damaged cells. This process usually slows down as we age, but low calorie diets make the body re-synthesize and turn over more cells - a situation associated with youth and good health. Dr. Spindler and his colleagues used their screening method to search for drugs which cause pre-cancerous and cancerous cells to commit suicide and to replace those cells with new, healthy cells. It is thought that the body does this because it normally kills some cells like damaged and rogue cancer cells to provide energy when it is starving. Then it replaces these cells when a meal is eaten.

A more detailed overview of the potential biochemical mechanisms behind CR’s beneficial health effects can be found in this March 2006 Scientific American article:

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With many baby boomers about to retire, maintaining independence and the ability to live an active, engaged retirement are top of mind. A recent study published in the Archives of Internal Medicine found that deficiencies in several micronutrients may increase the risk for having difficulty performing daily tasks as people age.

Specifically, the study looked at women over the age of 65 and found that deficiencies in selenium, vitamin B6, and vitamin B12 were all associated with significantly greater risk of experiencing disability, which was defined as self-reported difficulty in performing two or more activities such as bathing, dressing, toileting, transferring and eating.

Selenium is an essential trace mineral that is used by the body in important antioxidant-related enzymes. Selenium also plays an important role in immune function and may help to prevent the onset of certain cancers, such as prostate cancer.

Vitamin B6 and B12 are involved in important enzyme reactions, nervous system function, and help to maintain low homocysteine levels. High homocysteine levels are associated with oxidative stress, endothelial dysfunction, vascular diseases (heart disease, stroke), and, in particular, with decline of cognitive function.

Nutritionally, your best bet for avoiding the potential problems highlighted by this study are to follow a good diet, including mostly whole foods, lots of fresh vegetables & fruits, healthy fats, and lean protein sources.

Also, supplementation with a broad-based multi-vitamin/mineral containing at least 200 mcg selenium and the B vitamin equivalent of a B-50 complex, may help to ensure that you get adequate amounts of these essential nutrients on a regular basis and to prevent/delay the onset of disability. It’s important to select supplements containing both adequate and well-absorbed forms of the different nutrients.

A recent study in the Journal of the American Medical Association examined different midlife risk factors and their association with survival rates in men.

Researchers found that 42% of the study’s 5820 original study participants survived to the age of 85. However, only 11% of the study participants survived to 85 years without getting one of 6 major chronic diseases and without physical and cognitive impairment (a state referred to by the authors as “exceptional survival”).

Participants who had high (hand) grip strength and avoided risk factors, including:

• Becoming overweight
• High blood pressure
• High blood sugar
• Smoking
• Excessive alcohol consumption

in mid-life had a greater chance of both reaching age 85 and exceptional survival.

Being married and avoiding high triglycerides were also associated with exceptional survival. Being single, on the other hand, was not associated with reaching age 85.

Researchers estimated that the probability of survival to 85 may be as high as 69% for men with no risk factors and as low as 22% with six or more risk factors. Exceptional survival to age 85 was estimated as high as 55% for men with no risk factors and as low as 9% with six or more risk factors.

Those are some pretty big differences. Nutrition plays a significant role in many of the risk factors - e.g., high blood sugar, high blood pressure, and more. There’s clearly a lot that an individual can do well before reaching older age to both lengthen and improve the quality of life.

A couple of more studies just released that again suggest omega fatty acids may be helpful in slowing cognitive decline:

Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease

This study found that patients with very mild Alzheimer’s disease (AD) who supplemented with omega-3 fatty acids (2.3 g/day)experienced significantly slower rates of decline in mental function. However, individuals with mild to moderate AD didn’t improve.

This result reinforces the importance of early intervention and prevention. Once damage to the brain is significant (as seen in moderate cases of AD), a single helpful nutrient like omega-3 fats, although not detrimental, is likely to not necessarily lead to great improvement.

Dietary supplementation of arachidonic and docosahexaenoic acids improves cognitive dysfunction.

Arachidonic acid is an omega-6 fat, while docosahexaenoic acid (or DHA) is an omega-3 fat. Most people get plenty of omega-6 fats in the diet, as they are found in high quantities in vegetable oils used in processed and restaurant-prepared foods. Arachidonic acid (ARA) is also found in high amounts in red meat and egg yolks. On the other hand, most people are deficient in omega-3 fats, such as DHA and eicosapentaenoic acid (EPA), which are found in fish oil.

This second study found that individuals with mild cognitive impairment who supplemented with only 240 mg of ARA and DHA experienced improvements in both immediate memory and attention scores. As in the earlier study, no improvement was seen in individuals who had already developed AD.

For omega-3 fats DHA & EPA, it’s important to make sure that the source (fish or supplements) is low in contaminants, such as heavy metals and PCBs. Tested fish oil supplements are your best bet there.

You can learn more about the important roles of omega-3 fats in disease prevention and treatment here.

And, you can learn more about ways to preserve and improve cognitive function here.

Researchers at San Diego’s Scripps Research Institute recently published a study that found mice that were genetically altered to have a reduced core body temperature had a significantly greater average lifespan (12% in males, 20% in females) than non-altered mice.

In the past, other studies have noted that:

• Body temperature and aging are related in cold-blooded animals.
• Calorie-restriction (CR) can increase lifespan in warm-blooded animals and also results in a lowered body temperature.

However, this was the first study to find that a sustained decrease in core body temperature could increase lifespan in warm-blooded animals independently of calorie-restriction or an altered diet.

Prior to the current study, critical questions about the relation between calorie restriction, core body temperature, and lifespan remained unanswered. Was calorie restriction itself responsible for longer lifespan, with reduced body temperature simply a consequence? Or was the reduction of core body temperature a key contributor to the beneficial effects of calorie restriction?

To find out, the researchers genetically altered the mice to over-express a protein in the hypothalamus, the part of the brain responsible for regulating body temperature. This protein change increased the hypothalamus temperature, which, in turn, resulted in a decrease in body temperature of approximately 0.5 to 1.0 degree farenheit.

The altered mice had normal ability to generate fever and were just as active as the other mice. Most importantly, the altered mice were allowed to eat as much food as they wanted, and ate about the same as the control mice. They also weighed about 10 percent more than the control mice (less energy required to maintain the lower body temperature).

The exact mechanisms as to how the decrease in body temperature may lengthen life remain to be discovered (Hormonal effects? Reduced oxidative stress?), but this finding is certainly an interesting and important one. The results reinforce just how important those small structures at the base of your brain, like the hypothalamus, are to your overall health. Small changes in function can make big differences.

An announcement that didn’t make the major newspaper headlines, but is nevertheless big news. Researchers at the Linus Pauling Institute at Oregon State University (OSU) have discovered a new technique that allows them to observe and accurately measure the level of a key oxidant (superoxide) in animal cells.

Prior to this, there was no direct and accurate way to measure superoxide or its origin from the two places that produce it, the cell’s cytosol or mitochondria. Now there is.

With the new system developed at OSU, researchers can use a fluorescent microscope, a fairly standard laboratory tool, to actually see levels of superoxide and observe changes as experiments are performed with living cells.

Oxidation is a process that occurs naturally in the body — for example, in cell energy production and some immune reactions. As a result of the process, unstable atoms and molecules (e.g., free radicals such as superoxide) can be formed.

The body produces substances (e.g., glutathione, superoxide dismutase, catalase) that help to stabilize these atoms and molecules and prevent excessive damage and inflammation. We also take in anti-oxidants through our diet, in the form of different nutrients such as vitamins C and E, that help to neutralize these free radicals.

When these free radicals accumulate, cell structures can be damaged. This damage is believed to play an important role in many degenerative diseases, including ALS, Parkinson’s, Alzheimer’s, heart disease, hypertension, diabetes, and more.

The discovery of this technique will help researchers better understand what’s really happening in cells, as well as the effects of different potential treatments, and should help to speed research in many diseases. It’s definitely good news.