Posts tagged Health

Vitamin D conspiracy leads straight to Big Pharma

0
330 days
by in Health, Osteoporosis

You’ve probably heard about the bad rap vitamin D has been getting lately. The argument goes something like this…the vitamin D crisis isn’t as bad as we thought. You probably don’t need as much of it as we thought. But it’s a free country. So go ahead and take 400 IU of it per day, if you want. That’s more than enough. Just don’t go over 4,000 IU per day. “High doses” like that can increase your risk for “harm”

These new guidelines come from the U.S. Institute of Medicine (or IOM), a powerful non-profit agency that advises the nation of matters of health. But here’s the problem: Their report is pure propaganda.

In fact, I believe these low doses of vitamin D are a deliberate attempt to keep the American public needing more drugs until the day they die. (I’ll admit, that sounds a tad paranoid. But I’ll explain why my paranoia is well-founded a moment.)

First, let’s look at the three major problems with the IOM research.

Leave it to the IOM to redefine “majority”

First off, the IOM report states that the “majority” of adults living in the U.S. get enough vitamin D…and that’s just nonsense.

As you’ll recall, last week I told you about a major CDC study that found almost 80 percent of Americans don’t get enough vitamin D. Plus, another major study published late last year by researchers from the University of Tennessee came up with similar results. In fact, this time researchers found that 87 percent of the general population is mildly to severely deficient in vitamin D. Even the most conservative estimates put vitamin D deficiencies at about 50 percent of the population.

So how the IOM can confidently claim the “majority” of Americans get enough vitamin D, I have no idea!

Spend a minute in the sun each day

The IOM report also states that “North Americans need on average 400 International Units (IUs) of vitamin D per day. People age 71 and older may require as much as 800 IUs per day because of potential changes in people’s bodies as they age.”

Again, this is pure nonsense. But before I go any further, here’s a quick biochemistry primer…

The IOM says you only need 400 IU of vitamin D. But they actually mean 400 IU of vitamin D3 (or cholecalciferol). Your skin makes this natural form of vitamin D when exposed to sunlight. In fact, spending just 30 minutes in the sun without sunscreen, your skin will produce anywhere from 10,000 IU to 50,000 IU of D3! Plus, you can also take D3 as a supplement.

Next…

Vitamin D3 passes through your liver and it turns into a pre-hormone called 25-hydroxycholecalciferol. This is abbreviated as 25(OH)D.

When you get a vitamin D blood test, we really want to see how much 25(OH)D is in your blood. We measure 25(OH)D in nanomoles per liter or nmol/l.

Now, stick with me, because here’s where it gets interesting…

According to the IOM report, taking just 400 IU of vitamin D3 per day will give 97 percent of us a blood serum level of 50 nmol/l. And that level will protect us from fractures. Sounds okay, I guess. But let me put this another way to show you just how silly the IOM recommendation really is…

Let’s assume that your body makes 10,000 IU of D3 for every 30 minutes spent in the sun without sunscreen. (Most experts say you make at least twice that much…but let’s not get picky.) So, how long does it take for your body to make 400 IU of D3?

Hurray! Just 1.2 minutes in the sun! That’s all you need to keep your bones strong.

Is it me, or does that just sound wrong?

Well, here’s the good news. It isn’t just me. It is wrong. And there’s some solid scientific proof to back me up…

IOM gets their numbers wrong

Two major meta-analysis’ from 2009 found that 50 nmol/l of 25(OH)D in your blood isn’t enough to protect you from a fracture or a fall. In fact, 28 separate studies found that 50 nmol/l isn’t enough!

Plus, the International Osteoporosis Foundation recommends men and women have 75 nmol/l of 25(OH)D. This is what it takes to protect you from accidental falls and fractures. Lastly, numerous studies over the years show that the more 25(0H)D in your blood, the greater your bone density. But to get up to those higher levels of 25(OH)D, you need more D3.

Plus, here’s another interesting twist. The authors of the IOM report most likely knew about all this research…they just chose to ignore it.

You see, before publishing the new vitamin D guidelines, the IOM board consulted with Dr. Walter Willet. The board even thanked Dr. Willet at the end of their report.

So who’s Dr. Willet?

He’s a vitamin D expert and Chair of the Department of Nutrition at Harvard. He also co-wrote one of the 2009 reports on vitamin D I mentioned earlier. The IOM, however, ignored his findings.

But don’t feel bad, Dr. Willet. Yours isn’t the only research the IOM ignored…

IOM report ignores research on vitamin D and disease

Remember how I told you the IOM said 400 IU of D3 is enough to protect you against osteoporosis? Well, what about everything else…like cancer and heart disease?

In a press conference, IOM chair Dr. Catherine Ross said “We could not find solid evidence that consuming more [vitamin D] would protect the public from chronic disease ranging from cancer to diabetes to improved immune function.” And with that simple statement, Dr. Ross lost all credibility.

Here are some of the best studies linking vitamin D and major diseases:

Breast cancer: Women with vitamin D blood serum levels less than 50 nmol/mL are eight times more likely to develop an aggressive form of breast cancer.

Colon cancer: Men and women with the highest vitamin D levels cut their colon cancer risk by 40 percent.

Heart Disease & Stroke: Men and women with low vitamin D double their heart attack or stroke risk.

Cognitive decline: Older women with low vitamin D are twice as likely to suffer cognitive impairment.

Diabetes: A whopping 91 percent of diabetics have low levels of vitamin D in their blood. Plus, the less vitamin D in their blood, the greater their blood sugar problems.

And I’m just scratching the surface here! If you want to look at all the scientific data on vitamin D, the Vitamin D Council is a good place to start. They list the studies by disease, so you can see all the scientific data Dr. Catherine Ross and her colleagues missed.

In closing, there’s one last reason why the IOM report has the pungent smell of propaganda…

There’s a rat in the house

Glenville Jones, PhD is one of the authors of the IOM report. He’s a scientist and also the co-inventor of drug made by a company called Cytochroma. This drug is still in development…but what condition will they treat with their top-secret drug?

You got it.

Vitamin D deficiencies!

(I’m not making this stuff up. You can see the patent for yourself at the U.S. Patent Office website.)

Dr. Jones also sits on the scientific advisory board of a drug company called Receptor Therapeutics. These guys also made a synthetic vitamin D treatment for cancer…in fact THREE synthetic vitamin D treatments for cancer. (Drug companies use synthetic vitamin D because they can patent it and make a huge profit. You can’t patent natural vitamin D.)

Well, isn’t that so thoughtful…

You don’t need to take vitamin D. But if you do happen to get cancer…guess who plans to have a vitamin D drug you can take?

Here’s the bottom line for you: Ignore anything published by the IOM. Take up to 5,000 IU of natural vitamin D3 each day. And avoid anything made by Cytochroma and Receptor Therapeutics.

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Brain Food: How to Eat Smart

3
447 days
by in Health, Neuro-Protection

It’s common to resolve to lose weight, but any sane person dreads a diet’s dulling effect on the brain.

In fact, many studies have shown that counting calories, carbs or fat grams, is truly distracting to the point that it taxes short-term memory. But how we eat can affect our minds at more fundamental levels, too.

Whether you are seeking brain food for exams or just want to be at your sharpest ever day, here are five things you should know about feeding your brain:

1. Fuel it up

The brain, which accounts for 2 percent of our body weight, sucks down roughly 20 percent of our daily calories. A picky eater, it demands a constant supply of glucose primarily obtained from recently eaten carbohydrates (fruits, vegetables, grains etc.). Only in extreme instances of deprivation will the brain use other substances for fuel.

More recently evolved areas of the brain, such as the frontal cortex (it’s like the CEO of the brain), are particularly sensitive to falling glucose levels, while brain areas regulating vital functions are more hardy, said Leigh Gibson of Roehampton University in England. “When your glucose level drops, the symptom is confused thinking, not a change in breathing pattern,” he said.

This is not to suggest that we should constantly slurp soda to keep our brains functioning optimally. On the contrary, high glucose levels slowly but surely damage cells everywhere in the body, including those in the brain, said Marc Montminy of the Salk Institute for Biological Studies in California.

And according to a recent study published in the Oct. 3 issue of the journal Cell, by Dongsheng Cai and colleagues at the University of Wisconsin, the brain may react to excess food as if it were a pathogen. The resulting immune response, which occurs irrespective of weight gain, may cause cognitive deficits such as those associated with Alzheimer’s.

Similarly, high blood sugar, coupled with a cognitive task, is associated with elevated cortisol – a hormone known to impair memory in high doses, Gibson said. In other words, don’t get out the flash cards after that second (or third) piece of cake.

2. Become a grazer

The brain needs Goldilocks portions of energy: not too much, not too little.

To optimize brain power, Michael Green of Aston University in England suggests one tactic would be “more frequent but smaller meals.” The brain works best with about 25 grams of glucose circulating in the blood stream – about the amount found in a banana, said Gibson.

If trading three-meals-a-day for an all-day nibble seems unappealing, unpractical or simply anti-social, read on.

3. Eat lower on the glycemic index (GI)

The glycemic index ranks foods according to how they affect blood glucose levels. Pretzels are high on the index, because they cause blood sugar to rise very quickly. Raw carrots, by comparison, have a low glycemic ranking.

Carbs in lower glycemic food are broken into glucose molecules more slowly, thereby providing a steadier supply of energy to the brain. Low GI meals, gratefully, also best satiate hunger, writes J.M. Bourre of the French National Medicine Academy in the September 2006 issue of The Journal of Nutrition, Health and Aging.

High fiber carbohydrates are relatively low glycemic but combining them with fat or protein can slow absorption even more. For example, the traditional white Wonder Bread is high glycemic; it is digested quickly, causing a stressful, and brief, spike in glucose levels. Dark fiber-rich whole wheat bread is lower on the index; its spike is slightly less sharp. But add some meat or other protein to the bread and the glucose absorption rate becomes a gentle curve. Top it off with a little olive oil and presto: brain-friendly fuel masquerading as a tasty lunch.

The key is a balanced diet, where all macronutrients – carbohydrates, fats and proteins – are given their due, Green said.

4. Know your fats

Despite fat’s ability to lower the GI of a meal, not all fats are equal. Trans fats, common in fast food, are the worst. Saturated fats are not great. Unsaturated fat is the healthiest.

“People who eat diets high in saturated fat are more susceptible to cognitive deficits,” said Gibson. The increased likelihood of strokes is just one acute example. Rats that gorged on saturated fat for several weeks had obvious damage to the hippocampus – a brain area critical to memory formation, he said.

Still, “the brain is 60 percent fat,” Green said, and very low levels of cholesterol have been associated with depression, aggression and anti-social behavior. While most people in developed countries need to limit their fat intake, “zero fat is definitely not the way to go,” he said.

Essential fatty acids, such as Omega-3s, are proving valuable in treating depression and other psychiatric disorders, such as schizophrenia, as well as benefiting infant brain development, Green said. However, he added, the effect of supplements on a healthy adult brain is controversial. It may be best to stick to natural sources, such as cold-water fish, seeds and nuts.

5. Know yourself

Despite broad similarities, food affects everyone’s brain a little differently. For example, Gibson explained, extroverts are more likely to succumb to the “post-lunch dip” – that desire to nap, or chug coffee, mid-afternoon. And size matters: Children and the very thin may feel faint or grumpy due to low blood glucose faster than an average-sized adult, explained Montminy.

Thinking about brain food is wise. But overall nutritional habits are also important. People who chronically under-eat, over-exercise or regularly skip meals can become fuzzy-headed even after a minor dip in glucose. They become sensitized to not getting enough, Gibson said.

But with the Goldilocks approach, there is no need to diet to distraction. “Every single fad diet is total rubbish,” Green said, but there is merit to eating low glycemically.

By Robin Nixon, Special to LiveScience, posted: 07 January 2009 07:17 am ET

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Is science on the brink of creating the elixir of life?

0
461 days
by in Anti-aging, Health

Once I had a very odd dinner with an elderly and distinguished scientist who told me how he planned to live for ever – or at least for a very long time indeed.

We ate in his beautiful house by the sea in California. Our meal consisted of one bowl of rice each and a glass of water.

With this extreme diet, my host said – limiting himself to 800-1,000 calories a day (the average male is recommended to consume 2,500) – he hoped to stave off death for many more decades.

article-1319011-0B7DF3F7000005DC-816_468x663Eternally youthful: Cliff Richard, 69, appears toned and bare chested in his 2011 calendar

Such a regime was based on the well-established theory that by reducing calorie intake, people can dramatically increase their lifespans. This had been shown, after numerous scientific investigations, to work in animals from fruit flies to mice.

Professor Roy Walford, a biologist at UCLA, was 74 years of age when I met him. He had no doubt that extreme calorie restriction would work in people, too. However, despite his punishing diet, he was to die five years later from the auto-immune disorder Lou Gehrig’s disease.

Seventy-nine years was a little better than the three score years and ten which have been approximated as the human lot since Biblical times – but his innings only matched the average lifespan for an educated, middle-class white California male of his generation.

It is tempting, then, in the light of this story, to write off the theory that by eating the bare minimum we can slow the aging process.

But it seems Professor Walford was probably on to something, even if the fates conspired to ensure that he personally did not benefit from his diet thesis. For there is a growing scientific consensus that aging – against which humanity has been battling for millennia – might not be inevitable.

Of course, the quest for eternal youth has been led by charlatans, frauds and snake-oil salesmen through the ages. There is money to be made by promising the Holy Grail – as the questionable claims on the labels of countless anti-aging beauty products will attest.

For centuries, lotions and potions have been touted as elixirs of longevity. These have ranged from products containing monkey glands to injections of minced dog testicles.

Unsurprisingly, all have failed.

Still, the search continues. We have been told that exercise, red wine, chocolate, Vitamin C and various cocktails of antioxidants are the answers.

The latest elixir claim comes from scientists in Italy, who announced this week that mice given dietary supplements rich in three amino acids (similar to the concoctions favored by human bodybuilders) lived on average 12 per cent longer than mice fed on ordinary food. For humans, this would mean about an extra ten years of life.

And yet the world still awaits its first 125-year-old. The record stands at 122 years – achieved by Frenchwoman Jeanne Calment, who died in 1997.

But the truth is, charlatans apart, the aging process may be more amenable to change than was thought.

article-1319011-0B89E26E000005DC-721_224x245article-1319011-0B89E2DA000005DC-862_224x245

The search for the elixir of youth continues: Lotions, potions and cosmetic surgery are all used to keep us looking young (left). Within decades pills may be available which will delay the onset of aging and illness (right)

For a start, life expectancy (the number of years a newborn is predicted to live) is increasing by five hours a day in Britain. This means a baby born in five years time should live a year longer than a baby born today.

This is, for the most part, simply a result of better healthcare.

For evidence we need only look at the first big jump in life expectancy, which took place in the 19th century when infant mortality rates dropped because of improved diets, better medicine and proper sanitation.

We haven’t conquered age, it’s just that more and more of us are living to our full potential. But we may now be nearing a surprising breakthrough.

According to a new book, The Youth Pill, by health journalist David Stipp, in a few decades a number of pills may be available, which will help delay the onset of most serious illnesses by up to ten years.

This would give us at least five extra years of healthy old age and allow the 122-year barrier to be breached.

Until recently, those scientists working on increasing the longevity of fruit flies or mice have shied away from making claims that humans could benefit from their work on genetics.

But now, as Stipp points out, this attitude seems to be changing; more and more experts now say that human lifespan can be increased – and what’s more, they agree that it would be a good idea.

How we grew old, and why, was a mystery until recently. It was commonly supposed that our bodies simply wore out, like machines. But this wasn’t a good analogy.

Unlike most machines, our bodies are equipped with efficient repair systems that keep our cells healthy for decades.

In fact, we do not really start to ‘age’ at all until we are into our 20s. So, discovering why these mechanisms stop working as we enter middle and old-age is the key to understanding the aging process.

Aging is, after all, not entirely inevitable. Several organisms appear to hardly age at all and live for centuries.

article-1319011-0B49DF50000005DC-450_224x301article-1319011-0004801700000258-70_224x301

World’s oldest humans: Walter Breuning (left) is believed to be the world’s oldest man at 114 and celebrated his birthday last month. Frenchwoman Jeanne Calment (right) is considered the oldest person who ever lived, and has a birth certificate dated February 21, 1875. She died in 1997 aged 122

Humans are among the longest-lived of all species, but our longevity is exceeded by some giant tortoises which can live for nearly 200 years.

Bowhead whales have recently been found, alive and well, with antique harpoons embedded in their skulls which can be dated back to the 1790s. Some of these animals may be more than 300 years old.

There is a pattern in all this. Big creatures tend to live longer than small ones. Anything that can fly or swim tends to live longer than animals stuck on the ground.

Understanding these differences gives us our first clue as to how aging works – and to what might be done to delay it.

The evolutionary theory of aging states that animals age at a rate commensurate to their likely survival time in the wild. Mice age quickly because – being small and feeble – they are likely to be eaten, starve or perish due to cold before too long.

Evolution has given the mouse a body that literally lives fast and dies young. It’s full of sex hormones turbocharging its chances of reproducing before it is eaten by predators.

It makes little sense for a mouse to be equipped with, say, anti-cancer mechanisms, if the chances are that it will be an owl or cat’s dinner within a year or two.

Big creatures tend to live longer than small ones. Anything that can fly or swim tends to live longer than animals on the ground.

On the other hand, elephants age slowly because, being big, they are hard to kill. It takes a long time for them to die of starvation and they cope well when times get tough.

So elephant bodies have evolved complex DNA repair systems which can keep them going for half a century or more.

Birds also live a long time because, although small, they can fly and thus avoid predators.

Bats live longer than mice for the same reason, and porcupines and tortoises are long-lived simply because they make a difficult meal. In each case, their bodies age slowly to make the most of their potential life spans.

Still, knowing why we age tells us little about how we age – and even less about what we might be able to do about it.

There is growing evidence, however, that the very hormones that enable us to reproduce – those which produce eggs and sperm – may in themselves contribute to the aging process.

“Death,” said one biologist, “is the price we pay for sex.”

Advances in DNA analysis – reading the entire genetic codes of organisms – have opened up exciting new areas in aging research, allowing scientists to pinpoint individual genes which may be be responsible for the breakdown in our bodies over time.

Yet the reality is that many of the resulting “breakthroughs” have proved to be dead ends.

For decades, “free radicals” (waste chemicals produced by our bodies as by-products of respiration, digestion and the action of muscles) have been suggested as possible drivers of the aging process.

AYW45Particle-1319011-0B8231DF000005DC-545_224x292

Elephants age very slowly and cope well when times get tough. They have evolved complex DNA repair systems which can keep them going for half a century or more, while smaller animals like the mouse (right) live fast and die young

Some scientists have claimed that we should take large quantities of free-radical neutralizers called antioxidants (which include Vitamin C and are best found in fruit and vegetables).

Yet Vitamin C, it turns out, may actually increase free-radical damage and very large doses can interfere with the body’s natural repair mechanisms.

It is such contradictions that have led researchers to focus, instead, on calorific restriction.

Mice placed on near-starvation diets have seen their life expectancies increase 20-35 per cent. If such results were achievable in humans, the average Briton’s life expectancy would rise to almost 100 – with the potential to carry on to 150.

This is precisely what Professor Roy Walford was trying to achieve with his grimly tedious rice and water diet in California.

And the truth is that research into whether calorie restriction will greatly extend our lifespans would take decades to reach firm conclusions – simply because we are so much larger than mice.

Even so, research on rodents has uncovered how extreme calorie restriction appears to switch on a genetic mechanism called a stress response. This has evolved to allow animals to survive tough conditions (such as a very hard winter when little food is available).

It seems the bodies of mice – and possibly those of humans, too – react to starvation by boosting their repair mechanisms, triggering anti-inflammatory responses which slow the damage done to vital organs as they age.

The problem for humans is that near-starvation is unlikely to catch on. What people are much more likely to turn to are drugs which mimic the effects of extreme calorie restriction, without having to live on lettuce.

And such drugs may soon be available. One could be based on the chemical resveratrol which is a plant compound found in red wine.

In 2006, Harvard scientist David Sinclair found that this could activate a stress-response gene called SIR2 in mice which extended their lives.

Vast fortunes are being spent by the big drug firms on anti-aging drugs.

The happy fact that the elixir of youth is found in wine was suggested as the possible reason why the French, who eat a lot of supposedly unhealthy meat and cheese, smoke too much and drink a lot of alcohol, have one of the world’s highest life expectancies.

Then, last year, three teams of researchers in the U.S. reported that another chemical which mimics the effects of starvation, called rapamycin, makes mice live longer by suppressing the onset of cancer. The chemical was isolated from a fungus found on Easter Island in the Pacific.

Unsurprisingly, the big drug firms are trying to exploit these discoveries. Vast fortunes are being spent on anti-aging drugs which mimic calorie restriction.

The problem, skeptics point out, is that the aging mechanism in rodents may be quite different to the one in humans.

Cliff_2011_A3_calendar.inddThe Official 2011 Cliff Richard calendar is on sale in stationery stores or online at www.danilo.com

Therefore, resveratrol and similar chemicals may not prove to be the answer (the same may be true of the Mr Universe protein supplements trumpeted this week).

But the likelihood is that, in a few years, pills will be developed that will be able chemically to copy the effects of a near-starvation diet and that may well increase lifespan in humans.

If this happens, what would a world of 130-year-olds be like? Of course, there is a big difference between being a healthy 130-year-old and someone who has spent the last 40 years of their life suffering from dementia.

So what about the anti-aging pioneer Roy Walford? Ironically, his death was caused by a rare disease that is exacerbated, not ameliorated, by a low-calorie diet.

But if he was right, then by helping publicize what was once an obscure field of scientific research, his last, hungry years by the Pacific may not have been in vain.

www.dailymail.co.uk, Oct 14,2010, by By Michael Hanlon


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The Facts, Statistics and Dangers of Soda Pop

168
494 days
by in Health

Kids are heavy consumers of soft drinks, according to the U.S. Department of Agriculture, and they are guzzling soda pop at unprecedented rates.

Carbonated soda pop provides more added sugar in a typical 2-year-old toddler’s diet than cookies, candies and ice cream combined.

Fifty-six percent of 8-year-olds down soft drinks daily, and a third of teenage boys drink at least three cans of soda pop per day.

  • These popular beverages account for more than a quarter of all drinks consumed in the United States.
  • More than 15 billion gallons were sold in 2000.
  • That works out to at least one 12-ounce can per day for every man, woman and child.

Not only are soft drinks widely available everywhere, from fast food restaurants to video stores, they’re now sold in 60 percent of all public and private middle schools and high schools nationwide, according to the National Soft Drink Association. A few schools are even giving away soft drinks to students who buy school lunches.

As soda pop becomes the beverage of choice among the nation’s young – and as soda marketers focus on brand-building among younger and younger consumers – public health officials, school boards, parents, consumer groups and even the soft drink industry are faced with nagging questions:

  • How healthful are these beverages, which provide a lot calories, sugars and caffeine but no significant nutritional value?
  • And what happens if you drink a lot of them at a very young age?

Recently, representatives of the soft drink industry, concerned that public opinion and public policy may turn against them, will staged a three-day “fly-in” to lobby Congress to maintain soft drinks sales in schools; and to educate lawmakers on the “proper perspective” on soft drink use.

The industry plans to counter a US Department of Agriculture proposal, announced in January, that would require all foods sold in schools to meet federal nutrition standards. That would mean that snack foods and soft drinks would have to meet the same standards as school lunches.

Nearly everyone by now has heard the litany on the presumed health effects of soft drinks:

  • Obesity
  • Tooth decay
  • Caffeine dependence
  • Weakened bones

But does drinking soda pop really cause those things?

To help separate fact from fiction, the Health section reviewed the latest scientific findings and asked an array of experts on both sides of the debate to weigh in on the topic. Be forewarned, however: Compared with the data available on tobacco and even dietary fat, the scientific evidence on soft drinks is less developed. The results can be a lot like soft drinks themselves, both sweet and sticky.

Obesity

One very recent, independent, peer-reviewed study demonstrates a strong link between soda consumption and childhood obesity.

One previous industry-supported, unpublished study showed no link. Explanations of the mechanism by which soda may lead to obesity have not yet been proved, though the evidence for them is strong.

Many people have long assumed that soda – high in calories and sugar, low in nutrients – can make kids fat. But until this month there was no solid, scientific evidence demonstrating this.

Reporting in The Lancet, a British medical journal, a team of Harvard researchers presented the first evidence linking soft drink consumption to childhood obesity. They found that 12-year-olds who drank soft drinks regularly were more likely to be overweight than those who didn’t.

For each additional daily serving of sugar-sweetened soft drink consumed during the nearly two-year study, the risk of obesity increased 1.6 times.

Obesity experts called the Harvard findings important and praised the study for being prospective. In other words, the Harvard researchers spent 19 months following the children, rather than capturing a snapshot of data from just one day. It’s considered statistically more valuable to conduct a study over a long period of time.

Researchers found that schoolchildren who drank soft drinks consumed almost 200 more calories per day than their counterparts who didn’t down soft drinks. That finding helps support the notion that we don’t compensate well for calories in liquid form.

Tooth Decay

Here’s one health effect that even the soft drink industry admits, grudgingly, has merit. In a carefully worded statement, the NSDA says that “there’s no scientific evidence that consumption of sugars per se has any negative effect other than dental caries.” But the association also correctly notes that soft drinks aren’t the sole cause of tooth decay.

In fact, a lot of sugary foods, from fruit juices to candy and even raisins and other dried fruit, have what dentists refer to as “cariogenic properties,” which is to say they can cause tooth decay.

Okay, so how many more cavities are soft drink consumers likely to get compared with people who don’t drink soda? This is where it gets complicated.

A federally funded study of nearly 3,200 Americans 9 to 29 years old conducted between 1971 and 1974 showed a direct link between tooth decay and soft drinks. Numerous other studies have shown the same link throughout the world, from Sweden to Iraq.

But sugar isn’t the only ingredient in soft drinks that causes tooth problems. The acids in soda pop are also notorious for etching tooth enamel in ways that can lead to cavities. “Acid begins to dissolve tooth enamel in only 20 minutes,” notes the Ohio Dental Association in a release issued earlier this month.

Caffeine Dependence

The stimulant properties and dependence potential of caffeine in soda are well documented, as are their effects on children.

Ever tried going without your usual cup of java on the weekend? If so, you may have experienced a splitting headache, a slight rise in blood pressure, irritability and maybe even some stomach problems.

These well-documented symptoms describe the typical withdrawal process suffered by about half of regular caffeine consumers who go without their usual dose.

The soft drink industry agrees that caffeine causes the same effects in children as adults, but officials also note that there is wide variation in how people respond to caffeine. The simple solution, the industry says, is to choose a soda pop that is caffeine-free. All big soda makers offer products with either low or no caffeine.

That may be a good idea, though it raises the question of whether soda machines in schools should be permitted to offer caffeinated beverages or at least be obligated to offer a significant proportion of caffeine-free products.

It also raises the question of how one determines a product’s caffeine content. Nutrition labels are not required to divulge that information. If a beverage contains caffeine, it must be included in the ingredient list, but there’s no way to tell how much a beverage has, and there’s little logic or predictability to the way caffeine is deployed throughout a product line.

Okay, so most enlightened consumers already know that colas contain a fair amount of caffeine. It turns out to be 35 to 38 milligrams per 12-ounce can, or roughly 28 percent of the amount found in an 8-ounce cup of coffee. But few know that diet colas – usually chosen by those who are trying to dodge calories and/or sugar – often pack a lot more caffeine.

A 12-ounce can of Diet Coke, for example, has about 42 milligrams of caffeine – seven more than the same amount of Coke Classic. A can of Pepsi One has about 56 milligrams of caffeine – 18 milligrams more than both regular Pepsi and Diet Pepsi.

Even harder to figure out is the caffeine distribution in other flavors of soda pop. Many brands of root beer contain no caffeine. An exception is Barq’s, made by the Coca-Cola Co., which has has 23 milligrams per 12-ounce can. Sprite, 7-Up and ginger ale are caffeine-free. But Mountain Dew, the curiously named Mello Yellow, Sun Drop Regular, Jolt and diet as well as regular Sunkist orange soda all pack caffeine.

Caffeine occurs naturally in kola nuts, an ingredient of cola soft drinks. But why is this drug, which is known to create physical dependence, added to other soft drinks?

The industry line is that small amounts are added for taste, not for the drug’s power to sustain demand for the products that contain it. Caffeine’s bitter taste, they say, enhances other flavors. “It has been a part of almost every cola – and pepper-type beverage – since they were first formulated more than 100 years ago,” according to the National Soft Drink Association.

But recent blind taste tests conducted by Roland Griffiths at Johns Hopkins Medical Institutions in Baltimore found that only 8 percent of regular soft drink consumers could identify the difference between regular and caffeine-free soft drinks.

The study included only subjects who reported that they drank soft drinks mainly for their caffeine content. In other words, more than 90 percent of the self-diagnosed caffeine cravers in this small sample could not detect the presence of caffeine.

That’s why the great popularity of caffeinated soft drinks is driven not so much by subtle taste effects as by the mood-altering and physical dependence of caffeine that drives the daily self-administration.

And the unknown could be especially troublesome for the developing brains of children and adolescents. Logic dictates that when you are dependent on a drug, you are really upsetting the normal balances of neurochemistry in the brain. The fact that kids have withdrawal signs and symptoms when the caffeine is stopped is a good indication that something has been profoundly disturbed in the brain.

Exactly where that leads is anybody’s guess– which is to say there is little good research on the effects of caffeine on kids’ developing brains.

Bone Weakening

Animal studies demonstrate that phosphorus, a common ingredient in soda, can deplete bones of calcium.

And two recent human studies suggest that girls who drink more soda are more prone to broken bones. The industry denies that soda plays a role in bone weakening.

Animal studies – mostly involving rats – point to clear and consistent bone loss with the use of cola beverages. But as scientists like to point out, humans and rats are not exactly the same.

Even so, there’s been concern among the research community, public health officials and government agencies over the high phosphorus content in the US diet. Phosphorus – which occurs naturally in some foods and is used as an additive in many others – appears to weaken bones by promoting the loss of calcium. With less calcium available, the bones become more porous and prone to fracture.

The soft drink industry argues that the phosphoric acid in soda pop contributes only about 2 percent of the phosphorus in the typical US diet, with a 12-ounce can of soda pop averaging about 30 milligrams.

There’s growing concern that even a few cans of soda today can be damaging when they are consumed during the peak bone-building years of childhood and adolescence. A 1996 study published in the Journal of Nutrition by the FDA’s Office of Special Nutritionals noted that a pattern of high phosphorus/low calcium consumption, common in the American diet, is not conducive to optimizing peak bone mass in young women.

A 1994 Harvard study of bone fractures in teenage athletes found a strong association between cola beverage consumption and bone fractures in 14-year-old girls. The girls who drank cola were about five times more likely to suffer bone fractures than girls who didn’t consume soda pop.

Besides, to many researchers, the combination of rising obesity and bone weakening has the potential to synergistically undermine future health. Adolescents and kids don’t think long-term. But what happens when these soft-drinking people become young or middle-aged adults and they have osteoporosis, sedentary living and obesity?

By that time, switching to water, milk or fruit juice may be too little, too late.

Washington Post February 27, 2001

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Lithium increases gray matter in the brain

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by in Anti-aging, Health, Neuro-Protection

Able to stabilize the mood swings of many people with manic depression, lithium revolutionized psychiatric therapy when the drug came on the scene several decades ago. Yet neuroscientists remain perplexed at how this potent medication works.

Scientists in Detroit have now provided a clue that could help resolve that mystery. They find that about a month of treatment with the drug increases the volume of gray matter in a person’s brain. Gray matter, the so-called thinking part of the brain, is made up primarily of the main bodies of nerve cells and their short connections.

“This is a highly significant finding and may shed light on the therapeutic mechanism of lithium,” says De-Maw Chuang of the National Institute of Mental Health in Bethesda, Md.

Another study by some of the Detroit scientists hints that lithium stimulates production of new brain cells. This observation raises hope that the drug can treat strokes, Alzheimer’s disease, and other conditions that kill brain cells. It may also support a radical new theory that the birth and death of brain cells underlie depression.

There have been hints before that lithium safeguards nerve cells. Two years ago, Chuang’s group showed that the drug protects nerve cells from fatal over-stimulation by the brain chemical glutamate. Husseini K. Manji of Wayne State University in Detroit and his colleagues then found that lithium-treated nerve cells overproduce a protein, bcl-2, that helps cells resist signals to commit suicide.

Manji next joined with his colleague Gregory J. Moore to carry out a brain-imaging study of people starting lithium treatment for manic depression. After 4 weeks, about the time it takes for lithium’s mood-stabilizing effects to emerge, the drug had increased the volume of brain gray matter by about 3 percent in 8 of the 10 people studied, the researchers report this week at the Society for Neuroscience meeting in New Orleans.

“This is the first demonstration of a pharmacological increase of human brain matter,” says Moore.

The researchers propose that most of the increased volume results from nerve cells sprouting additional branches to nearby cells, a sign of healthy brain cells. A small part of the increased gray matter may even consist of new brain cells.

In New Orleans, Manji’s group reported that lithium boosted new nerve cell production in one brain region of rodents. Mice receiving lithium had about 25 percent more new brain cells in the hippocampus than untreated mice did.

In past mouse studies, a diverse slate of proven antidepressant therapies, including electroconvulsive therapy, exercise, and drugs such as Prozac, has triggered the birth of nerve cells in the hippocampus.

This earlier work and other evidence have prompted some scientists to theorize that depression stems from problems with a brain’s natural ability to generate new cells in the hippocampus. That remains speculation, however. Indeed, only recently have scientists accepted that the adult human brain can grow new cells.

Lithium‘s ability to protect nerve cells and increase production of new ones may make the drug useful in more illnesses than manic depression, suggests Moore. Chuang, for example, reported last year that lithium reduces brain-cell loss in a rodent version of Huntington’s disease.

The drug also protects rodent brains from cell death after a stroke, even if researchers wait to administer the drug. “We can give lithium up to 3 hours after the onset of stroke,” says Chuang.

Manji proposes testing lithium in people with Alzheimer’s and Parkinson’s diseases and amyotrophic lateral sclerosis, more commonly known as Lou Gehrig’s disease.

J. Travis, Reprinted from Science News

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