The BBC is carrying an article today about an experiment done for a television program in the United Kingdom.
Nine volunteers aged 36 to 49 set up home in a tented enclosure at Paignton Zoo, Devon, right next door to the ape house.
They were then put on what was essentially a vegan diet for a week followed by a vegan and fish diet for five days. They didn’t call it a vegan diet, choosing the more catchy name of an Evo Diet. The nutritionist who designed the eating plan was inspired by the diet consumed by apes in the wild.
She devised a three-day rotating menu of fruit, vegetables, nuts and honey. The prescribed menu was designed to be safe to eat raw; to meet adult human daily nutritional requirements; and it provided 2,300 calories – between the 2,000 recommended for women and 2,500 for men.
They typically ate 5kgs {Yes, ELEVEN POUNDS (!)} or 2,300 calories of fruit, vegetables, nuts and honey.
On a 3-day rota, they typically ate broccoli, carrots, radishes, cabbage, tomatoes, watercress, strawberries, apricots, bananas, mangoes, melons, figs, plums, oranges and hazelnuts.
Volunteers could also drink water. In the second week, standard portions of cooked oily fish were introduced. The idea was that this was to simulate the diet of a hunter gatherer.
Although this is really a mock experiment, it was a shame that they added the fish in the second week: it would have been nice to have seen the impact of just twelve days on a vegan diet.
Even so, the results were remarkable. The average cholesterol of the group fell by 23%, they lost an average of just under ten pounds and average blood pressures fell from 140/83 to 122/76.
I don’t find any of this at all surprising: I’ve done countless experimental diets on healthy volunteers, on patients and I’ve also tested them all on myself.
Eating the kind of diet to which we adapted over hundreds of millenia obviously makes good sense. And is far more likely to be successful than the latest fad diet based on some highly unnatural approach. The trouble with this experiment was that it actually did not simulate our ancestral diet: some – but not all – people do much better if they “eat with the seasons:” eating summer fruits in the summer, winter vegetables in the winter and so on. From what we know from the fossil record, it appears that our ancestors became omnivorous a very long time ago, and fish may have been a relatively recent addition to our diet.
Apart from those nit picky theoretical objections, the main problem with this diet is practical: it can be hard to carry around eleven pounds of fruit and vegetables. I’ve done it as part of an experiment, so I know that it is doable: it depends on how much you want to take control of your body.
There are, of course, loads of supplements for sale that claim to give you all the goodies packed into those eleven pounds of food, but in one convenient little pill. The trouble is that natural foods contain many other nutrients, not all of which have yet been identified. The bulk and the fiber are also important components of your diet.
The second problem is psychological: in Healing, Meaning and Purpose we spend a whole chapter/CD on methods for maintaining motivation and overcoming the psychological, social, subtle and even spiritual problems that often prevent us from looking after our bodies.
“As houses well stored with provisions are likely to be full of mice, so the bodies of those who eat much are full of diseases.”
–Diogenes (a.k.a. Diogenes Laertius, a.k.a. Diogenes the Cynic, Greek Philosopher and Founder of the Cynic School, c.412-323 B.C.E.)
“To become vegetarian is to step into the stream which leads to nirvana.”
–Buddha (a.k.a. “The Awakened”, a.k.a. Siddhartha Gautama, Indian Religious Figure and Founder of Buddhism, c.563 B.C.E. – c.483 B.C.E.)
“It’s bizarre that the produce manager is more important to my children’s health than the pediatrician.”
–Meryl Streep (American Emmy and Oscar-winning Actress, 1949-)
By a remarkable “coincidence,” less than a week after the appearance of two items (1. 2.) questioning the value of using genetic testing to help predict response to treatment in people suffering from depression, an important report has been released today.
The report is supported by a collaboration of the Agency for Healthcare Research and Quality and the Centers for Disease Control (CDC) and Prevention’s National Office of Public Health Genomics, and it was the CDC that funded it.
It is gratifying to see that the findings of the report are identical to those published in the two articles last week. The main conclusion of the report is that there is insufficient evidence to determine if current gene-based tests intended to personalize the dose of medications in a class of drugs called selective serotonin reuptake inhibitors (SSRIs) improve patient outcomes or aid in treatment decisions in the clinical setting.
The investigators reviewed 1,200 abstracts that led to the final inclusion of 37 articles. As we learned last week, the evidence indicates the existence of tests with high sensitivity and specificity for detecting only a few of the more common known polymorphisms of the cytochromes 2D6, 2C19, 2C8, 2C9, and 1A1.
They found mixed evidence regarding the association between CYP450 genotypes and SSRI metabolism, efficacy, and tolerability in the treatment of depression, mainly from a series of heterogeneous studies in small samples.
There were no data regarding:
- If testing for CYP450 polymorphisms in adults starting SSRI treatment for non-psychotic depression leads to improvement in outcomes versus not testing, or if testing results are useful in medical, personal, or public health decision making.
- If CYP450 testing influences depression management decisions by patients and providers in ways that could improve or worsen outcomes.
- If there are direct or indirect harms associated with testing for CYP450 polymorphisms or with subsequent management options.
This report confirms that there is little point in doing these genetic tests.
It also raises another point. It is now some years since some of these tests became available commercially. If they were really of value then we have to ask why there hasn’t been an avalanche of research on the topic – especially by the people marketing the tests – and why none of major psychopharmacology groups in the United States, Europe, Japan or Australia picked up on the tests. I probably know most of the people in these hospitals, universities and research centers and none has been much interested in this work.
So when someone suggests that you undergo some new test or investigation, remember to use your common sense. If there is only one person doing it – whether it’s a genetic test, a brain scan, some non-standard type of thyroid or adrenal test, or a Vega test – ask why nobody else is using it and why nobody has published any decent research on the method.
When it comes to your health use your common sense, your intuition and impartial information to be your guide and your support.
Within the last week we have talked about the association between Helicobacter pylori and Parkinson’s disease and the way in which Parkinson’s disease may often get better if people are treated with a cocktail of antibiotics. We have also discussed the association between Parkinson’s disease, allergies and inflammation.
Now new research from the University of North Carolina at Chapel Hill has found that people with low levels of LDL cholesterol are more likely to have Parkinson’s disease than people with high LDL levels. This is the form of cholesterol sometimes referred to as "bad cholesterol." This study followed the strange observation that people with Parkinson’s disease have a lower rates of heart attack and stroke than people who do not have the disease. It is also known that known that cigarette smoking, which increases a person’s risk for cardiovascular disease, is also associated with a decreased risk of Parkinson’s disease.
Few scientific stories are clear cut: it usually takes a while to get things right. Just to prove it, a study from the Netherlands found that high total cholesterol levels were associated with lower rates of Parkinson’s disease, but only in women.
So what to make of all this: infections, allergies and now cholesterol?
To try and understand this, I think that we need to introduce another actor to the stage. Since the early 1950s the medical community has been concerned about a striking concentration of amyotrophic lateral sclerosis (ALS) and Parkinsonism-dementia among the Chamorro people on the island of Guam. A number of lines of evidence have suggested that this group of illnesses has been caused by some neurotoxic agent in the environment, though nobody has been able to work out exactly what it is. One of the most attractive recent theories is that it might have something to do with toxins from Cycas plants. So the idea is that similar cholesterol-containing neurotoxins can come either from Helicobacter or from eating Cycas plants, or animals that have fed on the plants.
There is a complex inter-relationship between LDL- and HDL-cholesterol, and HDL-cholesterol appears to be anti-inflammatory: high levels of HDL-cholesterol are associated with low levels of inflammation. And it has recently been shown that simvastatin may cut the risk of developing Parkinson’s and Alzheimer’s diseases. Not just by lowering cholesterol but from its inflammatory activity.
It may also be that low levels of cholesterol may impair the activity of another factor: one that interests me is coenzyme Q10.
From a practical perspective, this new evidence reinforces a point that I made in Healing, Meaning and Purpose and on this blog: "boosting" one component of the blood or lowering another is not sensible. Whether dealing with cholecterol or immunity, we need to moduate and harmonize all the systems of our bodies and our minds.
Follow our systems for modulating the inflammatory mediators in your body and that alone should – theoretically – reduce your risk of many illnesses.
I shall keep you posted as this story continues to develop.
Posted by Richard G. Petty, MD on December 20, 2006 · 4 Comments
I have commented before that the increasing rates of multiple sclerosis as we move away from the equator has lead to speculation that it might have something to do with lack of sunlight and therefore reduced production of vitamin D in the skin.
A lack of vitamin D may also explain the increased rates of both type 1 and type 2 diabetes, as well as cluster headache at higher latitudes.
Vitamin D is not a single vitamin, but is instead a group of fat-soluble prohormones as well as the metabolites and analogues of these substances. There are two major forms of vitamin D: D2 (or ergocalciferol) and D3 or cholecalciferol. Vitamin D3 is produced in skin exposed to sunlight, specifically ultraviolet B radiation. Very few foods are naturally rich in vitamin D, and most vitamin D intake is in the form of fortified products including milk and cereal grains.
It used to be that we all made plenty of Vitamin D simply by being outside in the sun, but our time outside has been steadily falling since the beginning of the Industrial Revolution, and there are the increasing concerns about exposure to sunlight and some skin cancers.
Vitamin D is involved in many critically important chemcial reactions in the body, and Vitamin D receptors are found in cells in most organs in the body, including the brain, heart, skin, gonads, prostate, and breast. Apart from its effects on regulating calcium and phosphorus, Vitamin D is involved in maintaining the integrity of cell membranes and in modulating the immune system. There is some evidence that a modest increase in Vitamin D intake may reduce the risk of colon, breast and ovarian cancers.
There is a risk of overdosing with Vitamin D. The U.S. Dietary Reference Intake
Tolerable Upper Intake Level (UL) of vitamin D for childern and adults
is 50 micrograms/day (2000 IU/day). In adults, a daily intake of 2500
μg/day (100,000 IU) can, over a period of weeks and months, produce toxicity and, if
taken for years, as little as 50 to 75 μg/day (2000 to 3000 IU) can
produce toxicity.
In this week’s issue of the Journal of the American Medical Association, there is an important report that endorses everything that we have been saying. Researchers from
several prominent institutions in the United States have examined the
hypothesis that higher levels of 25-hydroxyvitamin D are associated
with a lower risk of multiple sclerosis.
The study confirmed the hypothesis: the risk of multiple sclerosis (MS) fell as blood levels of the vitamin rose.
The researchers uncovered 257 cases of MS among more than seven million military personnel who had given blood samples to the US Department of Defense.
Amongst white personnel, there was a 41% decrease in MS risk for every 50 nanomoles per litre increase in 25-hydroxyvitamin D, the key form of the vitamin found in the blood.
Those whose vitamin level was in the top 20% had a 62% lower risk of MS than those whose level was in the bottom 20%.
The researchers found no such association among black and hispanic personnel, but this could be a reflection of the smaller size of these sample groups.
This new research ties in with other work that has shown that Vitamin D supplements can prevent or favourably affect the course of a disease similar to MS in mice, as well as evidence that if you live in the Northern Hemisphere, being born in May is associated with a lower risk of MS than if you were born in the winter. If you are born in May, your mother will probably have been exposed to more sunlight – and therefore have produced more Vitamin D – during the later part of pregnancy when the final development of the nervous system takes place. Or alternatively you may have had a heathy dose of sunlight in the weeks immediately after your birth.
It is most likely that the Vitamin D helps by modulating the immune system and suppressing autoimmune reactions caused by specialised T helper 1 cells attacking myelin, the insulating material that sheathes most nerves. It is these attacks that are thought by most experts to play a key role in the development of MS.
If confirmed, the finding suggests that many cases of MS could be prevented or its severity reduced by increasing our levels of Vitamin D.
The data also confirm a point that we have made before: we should not be aiming to "boost" our immune systems, but to "modulate" them.
If you see an advertisement for some potion that is supposed to boost your immune system to help you ward off colds, the flu or something more serious, be suspicious: if the seller does not know the difference between boosting and modulating, it would be best to move on.
Your humble reporter was fascinated to read about some new research using the anti-malarial agent chloroquine as a potential treatment for the insulin resistance syndrome.
I have a personal reason for being interested. Hypoglycemia (low blood glucose) is an occasional feature of treatment with chloroquine and in 1980 a study first indicated that chloroquine might slow the break down of insulin by the liver. In the early 1980s there were a flurry of papers indicating that chloroquine did some subtle things to insulin and insulin receptors in many tissues. So we came up with the idea of measuring its effects in humans. There was a memorable occasion on which I was doing an outpatient clinic with an intravenous line in my arm. (English doctors are well known for doing experiments on themselves: I had a professor in medical school who said that you should never do to a patient what you haven’t had done to yourself. I shall leave it to you, gentle reader, to wonder if I’ve tried everything….).
So there I am doing my clinic when, around 11AM I begin to feel really strange: my glucose level was almost unrecordable and my insulin level was off the chart. Nothing that couldn’t be solved with a large dollop of sugar, but it made me very sympathetic to people who get hypoglycemic from their regular treatments.
Sometimes Nature does our experiments for us: we did a lot of work on diabetes because it is associated with high rates of vascular disease. So understanding the mechanisms by which diabetes does that may help illuminate some of the cellular disturbances underlying arteriosclerosis in general. We are also interested in the few illnesses in which a single disturbed gene may lead to a definable set of signs and symptoms. There is a rare illness known as ataxia telangiectasia in which sufferers have a high risk of developing some cancers particularly lymphomas and leukemia. People with the illness are very sensitive to ionizing radiation, have a specific type of immune deficiency, degeneration of parts of the brain related to muscle function and coordination and they age prematurely. More than ten years ago it was discovered that a single gene – ataxia-telangiectasia mutated (ATM) gene – was responsible for the illness. The gene is responsible for producing a protein that recognizes damage to DNA. It now seems that ATM may also be linked to metabolic and cardiovascular diseases. It does this by inhibiting a protein called JNK, a stress kinase involved in inflammation with related effects in insulin resistance and atherosclerosis. So to everyone’s surprise a gene that can cause a rare disease can also cause insulin resistance.
In the November issue of Cell Metabolism, researchers at Washington University School of Medicine in St. Louis and St. Jude Children’s Research Hospital in Memphis, Tennessee report that a small dose of chloroquine eased many symptoms of metabolic syndrome in mice, reducing blood pressure, decreasing hardening and narrowing of the arteries and improving blood sugar tolerance. The results suggest we may only need very low and perhaps infrequent doses of chloroquine to achieve similar effects in humans. Both insulin and chloroquine activate the ATM gene.
This adds to the data that some of the metabolic dysfunctions triggered by obesity may be linked to the inflammatory responses that go wrong in autoimmune disorders like arthritis and systemic lupus erythematosus.
And an older treatment for rheumatoid and lupus just happens to be chloroquine.
Chloroquine itself has some side effects, but this is important information that will help us design more effective and carefully targeted holistic treatments for both metabolic disturbances and inflammatory conditions. All in all, very good news indeed.
In Healing, Meaning and Purpose, I discuss some of the evidence for four previously little recognized causes of obesity:
- Stress
- Salt intake
- Pesticides
- Viruses
Each of these has been widely discussed in the professional literature, but little has percolated out into the general population except in advertisements for agents like Cortislim. I remain skeptical about these products. Tinkering with just one of the 260 hormones and neurotransmitters implicated in the control of weight is unlikely to be crowned with success. And their ingredients may also have the potential for causing problems. Recent advertisements have also mentioned that one of these products may elevate mood. Sad to say, in the last year we have seen two people who developed manic symptoms after taking one of the supplements. We are urging colleagues to see if there are any other cases, or whether these two were just coincidental.
I recently mentioned some of the evidence for viruses as a cause of weight gain.
Now a new publication from the Universities of Helsinki and Kuopio is out in this month’s journal Progress in Cardiovascular Diseases, that provides powerful support for the salt hypothesis.
The researchers report that an average 30-35 % reduction in salt intake during 30 years in Finland was associated with an extraordinary 75 % to 80 % decrease in both stroke and coronary heart disease mortality in the population under 65 years. During the same period the life expectancy of both male and female Finns increased by 6 to 7 years.
As expected, reducing salt intake has a beneficial effect on blood pressure.
But in my view the most interesting finding of the study is the close link between salt intake and obesity.
As bartenders, pub landlords and tavern owners have known since the beginning of time, increasing a person’s intake of sodium produces a progressive increase in thirst. (You didn’t think that those peanuts on the bar were put there out of the goodness of the establishment’s heart did you??!)
The progressive increase in the average intake of salt explains the observed increase in the intake of sugar-containing beverages which, in turn, has caused a marked net increase in the intake of calories during the same period in the United States.
Here is an extraordinary statistic: Between 1977 and 2001, energy intake from sweetened beverages increased on the average by 135 % in the United States. During the same period, the energy intake from milk was reduced by 38 %. The net effect on energy intake was a 278 kcal increase per person a day. The American Heart Association has estimated that, to burn the average increase of 278 kcal a day and avoid the development or worsening of obesity, each American should now walk or vacuum 1 hour 10 minutes more every day than in 1977. As we all know, that has not happened.
In the decade from 1976-1980 to 1988-1994 the overall prevalence of obesity increased 61 % among men and 52 % among women. During 1999 to 2002, the prevalence of obesity was 120 % higher among men and 99 % higher among women as compared with the 1976 to 1980 figures. The increased intake of salt, through induction of thirst with increased intake of high-energy beverages has clearly made a significant contribution to the increase of obesity in the United States.
It is also of note that until 1983 the use of salt did not change or even showed a continuous decreasing trend in the United States. The prevalence of obesity was relatively low and remained essentially unchanged from early 1960s to early 1980s.
This new study suggests that a comprehensive reduction in salt intake, which would reduce the intake of high-energy beverages, would be a potentially powerful means in the so far failed attempts to combat obesity in industrialized societies.
There is now conclusive population-wide evidence that indicates that we could achieve powerful beneficial health effects simply by reducing our overall salt intake. These benefits include a decrease in obesity.
As an aside, the population-wide long-term experience from Finland indicated that a remarkable decrease in the salt intake has not caused any adverse effects.
A number of years ago we were engaged in some experiments in which we replaced regular table salt – sodium chloride – with potassium chloride. For the first three weeks food seemed rather tasteless. But then we all suddenly discovered a new universe of flavors that had previously been hidden under a thick coating of salt. So a dietary change does have a temporary effect on your taste buds.
Although the paper doesn’t say so, there is also some data that salt may itself increase cortisol release.
The bottom line?
We now have clear, empirical data to support three out of the four points that I made in Healing, Meaning and Purpose, and there is some less robust data for the fourth.
I urge you to try gradually to reduce your personal intake or salt, and to encourage your family and friends to do the same. I mentioned that food may initially seem a little less flavorful, but then things change rapidly and for the better.
And your body will love you for the change!
Renal cell carcinoma (RCC) is the most common type of kidney cancer, and accounts for 2 percent of all adult cancers. It has been known for some time that diet plays a role in RCC risk, but attempts to identify which foods have harmful or beneficial effects have been inconclusive.
The smart money has been on foods that elevate insulin levels, because RCC is one of the cancers associated with obesity, and some RCC cell lines grow when exposed to insulin or insulin-like growth factors.
A new study by researchers form the Institute of Pharmacological Research "Mario Negri" in Milan, conducted a large case-control study of 2301 Italians. They found a significant association between high bread consumption and renal cell carcinoma. Eating a lot of pasta and rice may also raise the risk, while eating many vegetables may lower the risk. The study published online October 20, 2006 in the International Journal of Cancer, the official journal of the International Union Against Cancer (UICC), and is available via Wiley InterScience.
The researchers enrolled 767 adults diagnosed with RCC and 1534 controls who did not have the disease between 1992 and 2004. Two controls were matched to each case by gender, age range, and location. The researchers collected sociodemographic information, height, weight, lifestyle habits and personal and family medical history from each participant. They also administered a 78-item food frequency questionnaire which asked about the average weekly consumption for each item over the previous two years. They then performed statistical analyses to discover odds ratios (OR) with a 95 percent confidence interval.
They found a significant direct association was observed for bread consumption and a higher RCC risk. A modest non-significant risk increase was also observed for pasta and rice. On the other hand an increasing intake of poultry, processed meat, and all vegetables, both raw and cooked, all reduced the risk of RCC.
These findings confirm our guess about insulin and/or insulin-like growth factors. This association between elevated cereal intake (bread, pasta and rice) is most likely due to the high glycemic index of these foods, leading to an over-production of insulin and insulin-like growth factors.
The inverse relationship between vegetable consumption is consistent with previous studies and may be related to their content of vitamins, micronutrients or elements such as carotenoids, flavonoids and phytosterols.
This is not a perfect study: it is limited by the fact that the interviewers who gathered each participant’s information and administered the food questionnaire were not blind to who was who. But its big strengths include the sample size and the reproducibility and validity of diet information.
This study is important and speaks to the point that we have made before: a balanced diet is key, and your body does not want to be exposed to constant variations in glucose or insulin.
It also confirms all the advice that we have been offering you about what and when to eat. Click on the links to review what I have said before!
I think that everyone knows that breastfeeding confers considerable advantages on a baby. So much so that the American Academy of Pediatrics recommends exclusive breastfeeding for the first six months of life. Though some mothers cannot manage this for a whole range of reasons, and it’s always a real shame when women are made to feel guilty if they cannot breastfeed.
Amongst some of the likely health benefits for both mother a baby:
- Mother and child are more likely to bond
- A reduced risk of the child developing some respiratory problems, ear infections and gastrointestinal problems
- A reduced risk of developing allergies later in life
- A reduced risk of obesity in adulthood
- A reduced rate of attention deficit disorder
- A reduced risk of developing type I diabetes
- There may also be a reduced risk of developing osteoporosis in later life
- The mother has a reduced level of stress and postpartum bleeding
- Mothers who breastfeed have a slightly reduced risk of some types of cancer
To this list we can add that breastfed children are more intelligent. That is not a new discovery. It was first reported in the 1920s. A new study published in the British Medical Journal has re-examined the question. Most of the earlier studies failed to consider the mother’s intelligence, despite the well-recognized association between maternal education and breastfeeding. That association often breaks down in professional women who have to go straight back to work after giving birth, but it remains a key variable.
The researchers examined data from 3,161 mothers and 5,475 children, who were followed in a twenty-five year prospective study. Premature babies were excluded and the children’s’ intelligence was measured up to age five.
The breastfed babies had slightly higher IQs, but the effect was entirely accounted for by their mothers’ intelligence. Breastfeeding itself had little or no effect on intelligence scores. The mothers of the breast-fed children tended to be older and to be more likely to provide the growing child with a stimulating and supportive home environment.
In a separate study from the Australian Raine Study at the Telethon Institute for Child Health Research, that has tracked the growth and development of more than 2500 West Australian children over the past 16 years, it now emerges that children who were breastfed for longer than six months have significantly better mental health in childhood.
Children that were breastfed had particularly lower rates of delinquent, aggressive and anti-social behavior, and overall were less depressed, anxious or withdrawn. This makes sense: apart from the psychological impact of having a mother who is willing and able to breastfeed, breast milk is a rich source of polyunsaturated fatty acids – examples include docosahexaenoic acid and arachidonic acid – that are important for brain development and the growth of nerve cells.
There is also evidence that breastfeeding may reduce the risk of developing schizophrenia later in life, although it is difficult to be sure if it because of the breast milk itself or the kinds of mothers who breastfeed.
Posted by Richard G. Petty, MD on September 27, 2006 · Leave a Comment
If you are anything like me, you probably find loads of adverts in your mailbox for magical ways to lose weight, either by using some form of the Atkins diet, manipulating cortisol (it doesn’t work), or by paying attention to the glycemic index of the food that you eat.
Last January I summarized some of the recent research that showed that glycemic index and glycemic load were not related to measures of insulin sensitivity or secretion, or to the amount of fat in the body. However, the intake of fiber in the diet was found to have beneficial effects on insulin sensitivity, adiposity and the secretion of insulin by the pancreas. I went on to give some uncontroversial advice on how to eat.
Nobody thought that the glycemic index issue was dead: insulin and the other hormones involved in fat and carbohydrate metabolism are powerful and have multiple roles in the body.
A study published in the Archives of Internal Medicine in July, helps further refine our understanding about glycemic index. High carbohydrate foods with a low glycemic index are the best way to reduce your risk of cardiovascular disease. The problem is that you want to avoid sudden surges in glucose after you eat a meal. What normally happens is that those surges are accompanied by sudden rises in triglycerides and insulin. The three together can cause all kinds of mischief to the insides of your blood vessels. High protein and low glycemic index diets will help with weight, but it’s only the combinations of high carbohydrates with low glycemic index that reduces the risk of vascular disease.
My redoubtable Web Mistress, Carol Kirshner, has found a most useful resource at the University of Sydney, that you can use to help guide your food choices.
This is such a useful resource that we are going to attach it to our blogs and websites.
However, it’s essential that we don’t get seduced by the idea that high carbohydrate/low glycemic index eating is the solution to all of our ills.
We still need to follow the basic principles of a balanced diet:
- It is important for you to maintain your energy balance, between input and output
- Calories do count
- What you include in your diet is as important as what you exclude: we are designed to consume not just rice and lettuce, but an array of other nutrients
- Make only moderate dietary changes at any time: making big dietary changes can be a violent attack on your body and your mind
- Avoid the “trans-fatty acids”
- Try to consume some Mercury-free omega-3 fatty acids every single day
- Eat fewer simple carbohydrates
- Use weight management and exercise strategies that enhance your overall health and well-being
- Take more exercise: even small amounts can have a big effect.
- Make it a goal to gradually reduction your overall intake of cereals
Posted by Richard G. Petty, MD on September 21, 2006 · Leave a Comment
Retinoic acid is an organic compound derived from Vitamin A, that is involved in the development of the brain and in normal visual function. It is because of the involvement in the formation of the brain that medicine containing retinoic acid like compounds must not be given to women who could become pregnant.
In recent years it has become clear that it is also involved in the function of the mature nervous system, and there have been suggestions that it may have a role in illnesses life Alzheimer’s disease and schizophrenia.
One of the big breakthroughs in skin care was the introduction, in 1982, of a form of retinoic acid – isoretinoin – for the treatment of severe acne. It is marketed as Accutane in the USA and Roaccutane in the United Kingdom. Since its introduction there have been claims that it has caused depression and suicide in some patients taking it. The package insert specifically mentions this possible association. The trouble has been trying to sort out whether people taking it for acne became depressed because of the acne, whether it was the drug, or whether it was a chance association. 13 million patients have taken it world-wide, so sadly some depression might occur by chance.
That it was the drug causing the problem was supported by reports of people developing depression within days of starting the medicine. But it’s always difficult to go from association to causality. After all, it has not been possible to prove that smoking causes lung cancer, though nobody doubts it, becuase the association between the two is so strong.
The Medicines and Healthcare products Regulatory Agency had received 1,588 reports of suspected adverse events experienced by people taking the drug up to this month. This included 25 people who died from suicide.
Now a paper in the journal Neuropsychopharmacology has added substantial support the the notion that the medicine may cause depression. The researchers gave a form of retinoic acid to adolescent mice. They found that while there was no change in the physical abilities of the mice, the rodents spent significantly more time immobile in a range of laboratory assessments designed to test their response to stress.
This was interpreted as a sign that the animals were exhibiting signs of depression.
It’s difficult to extrapolate from mice to humans, and this certainly does not nail down the problem. It also does not mean that people should stop their treatment: this medicine works. But it emphasizes the importance of doing what the package insert says: watching young people with acne who are on treatment for any signs of depression.
