“The routine use of ultrasound in pregnancy is the biggest uncontrolled experiment in history.”
Beverly Beech, birth activist

In the first article in this series on natural childbirth, I presented evidence that – contrary to popular belief – hospital birth is no safer than home birth.

I’d like to begin this next article by telling you what it is not. It is not a blanket condemnation of ultrasound, nor is it a judgment of women who choose routine ultrasound during their pregnancy. It is not an argument against using ultrasound to investigate suspected problems, or to detect potential abnormalities, provided the woman is adequately informed.

The purpose of this article is to clarify the issues surrounding ultrasound’s use in clinical practice, to critically examine the clinical benefit of routine prenatal ultrasound, and to raise awareness of the potential risks associated with repeated ultrasound scans.

This was going to be a very long article, so I decided to split it into two parts. In part A I will discuss the use of ultrasound in clinical practice and examine whether it improves birth outcomes. In part B, I will review studies on the safety of ultrasound as it is used today, and make recommendations for expecting mothers.

History of ultrasound and use in clinical practice

Ultrasound was originally developed in WWII to detect enemy submarines. After the war in 1955, a surgeon in Glasgow named Ian Donald began to experiment with it for medical uses. Using beefsteaks as “control” subjects, he scanned the abdominal tumors he had removed from his patients and found that different tissues gave different patterns of sound wave echo. He quickly realized the potential of ultrasound for examining a growing baby in utero.

Initially, ultrasound was used only to investigate possible problems. For example, if there was bleeding in early pregnancy, it would be used to determine whether miscarriage was inevitable. Later in pregnancy, if breech or twins were suspected, ultrasound would be used to confirm that suspicion. In these cases, ultrasound can be very useful for a woman and her caregivers.

However, over the years ultrasound has come to be used as routine scan at 18-20 weeks for all women. This is referred to as “routine prenatal ultrasound”, or RPU for short. It involves scanning all pregnant women – whether a problem is suspected or not – in the hope of improving birth outcomes.

As often happens in medicine, techniques which may be of value to a small percentage of people slowly become adopted for routine use without prior study of benefits. A perfect example of this is the alarmingly common prescription of statin drugs for women, children and men without pre-existing heart disease, in spite of the fact that they’ve only been shown to be effective for a small segment of the population: middle-aged men with pre-existing heart disease.

The problem with this approach, of course, is that when we perform a procedure or administer a treatment to a segment of the population without properly testing it beforehand, we are essentially conducting an uncontrolled scientific experiment on that population – often without their understanding and consent. And in this case, we are performing that uncontrolled experiment on two of the most vulnerable populations: pregnant women and babies in the womb.

Some physicians and researchers have been questioning the wisdom of performing such an experiment for decades. In 1987, UK radiologist H.B. Meire remarked:

The casual observer might be forgiven for wondering why the medical profession is now involved in the wholesale examination of pregnant patients with machines emanating vastly different powers of energy which is not proven to be harmless to obtain information which is not proven to be of any clinical value by operators who are not certified as competent to perform the operations.

More recently, in 2010, the prestigious Cochrane Collaboration reviewed the available evidence on routine prenatal ultrasound (RPU) and concluded:

Existing evidence does not provide conclusive evidence that the use of routine umbilical artery Doppler ultrasound, or combination of umbilical and uterine artery Doppler ultrasound in low-risk or unselected populations benefits either mother or baby.

Despite the lack of evidence supporting RPU’s use in clinical practice, ultrasound is almost universally seen as a safe and effective procedure, and scans have become a “rite of passage” (in the words of Sarah Buckley) for pregnant women in most developed countries.

In the U.S., an estimated 65 to 70 percent of pregnant women have a formal scan in a diagnostic clinic, and many more women are scanned by their OB/GYN as part of their pregnancy visit.

Is ultrasound as effective and safe as we’ve been led to believe?

In order to answer that question, we have to distinguish between different uses of ultrasound. As I said earlier, ultrasound scanning can be a useful diagnostic tool when abnormalities are suspected. I have no argument with using it in this manner. The question I’d like to investigate here is whether routine prenatal ultrasound – when no abnormalities are suspected – is necessary and effective.

RPU is used today for several reasons:

1. To predict the birth due date
2. To determine the sex of the baby
3. To detect potential abnormalities
4. To identify placenta previa (low lying placenta)
5. To assess specific markers, such as the length of woman’s cervix and the amount of amniotic fluid at the end of pregnancy

It’s almost as if all pregnancies are immediately suspected to be abnormal until proven otherwise. In the words of TM Marteau ¹:

“Before the development of prenatal testing for fetal abnormality the fetus was assumed to be healthy, unless there was evidence to the contrary. The presence of prenatal testing and monitoring shifts the balance towards having to prove the health or normality of a fetus.”

The important question is: is RPU necessary and effective for these uses? Does it improve specific birth outcomes like perinatal mortality or morbidity?

Routine prenatal ultrasound is not recommended by researchers and major organizations

In general, RPU is accurate for predicting birth date when scans are performed in the early stages of pregnancy. The estimated due date (EDD) calculated by a scan at 7-8 weeks will be accurate to plus or minus 3-4 days.

However, calculations of EDD based on a woman’s menstrual cycle can be just as accurate.

What about detecting abnormalities? Studies show that RPU detects between 35-80% of the 1 in 50 babies that have significant abnormalities at birth. The larger centers with better trained sonographers have rates toward the higher end of the scale, but even major centers miss 40% of abnormalities.

That’s because many abnormalities are difficult or impossible to detect with RPU. Heart and kidney problems are unlikely to be picked up, as are some markers for Down syndrome. Cerebral palsy, autism, and other markers of intellectual disability are impossible to detect.

Then there’s the small but significant chance that an abnormal finding may be a false positive. A UK survey showed that for 1 in 200 babies aborted for supposed major abnormalities, the diagnosis on post-mortem was less severe than predicted by ultrasound, and the termination was probably unjustified. In the same survey, 2.4 percent of babies diagnosed with major malformations – but not aborted – had conditions that were significantly over- or underdiagnosed.

Two other studies have shown false positive results in roughly 10% of babies diagnosed with structural abnormalities. And in some cases, the abnormalities spontaneously resolve without intervention.

In addition to false positives, there are also cases that are difficult to interpret, and the outcome for the baby is unknown. This uncertainty can cause considerable stress and anxiety for the mother, which in turn adversely affects the developing baby. In one study involving women at higher risk, a full 10 percent of scans were uncertain. And in that same study, mothers with uncertain diagnoses were still anxious three months after the birth of their baby.

Ultrasound scanning for placenta previa is mostly accurate, but almost all women who test positive for it on a scan will be unnecessarily worried. Studies show that the placenta will move up and not cause problems during birth for 80 to 100 percent of women, and that detection of placenta previa by RPU is not safer than detection during labor.

All of this might explain why organizations like the American College of Obstetricians and Gynecologists recommend scans only for specific reasons, including uncertain due dates and fetal assessment, and advises that routine prenatal scans are cost-effective only when done by ultrasound technicians working in high-level centers.

In Canada, practice guidelines recommend only a single midpregnancy scan and stress that information on risks and benefits must be provided and informed consent obtained.

Routine prenatal ultrasound does not improve birth outcomes

Studies on RPU over the years have consistently shown that it does not improve birth outcomes as measured by clinical endpoints such as perinatal mortality and morbidity.

A 1993 meta-analysis of all randomized trials prior to that date covering 16,000 births showed no improvement in the condition of babies measured by APGAR score when ultrasound was used compared to those who did not have it. There was a slight reduction in perinatal mortality in this study. However, this happened because these babies were aborted during pregnancy – not because their lives were saved. There was no increase in the number of live, healthy births from RPU.

The authors of this study concluded:

Routine ultrasound scanning does not improve the outcome of pregnancy in terms of an increased number of live births or of reduced perinatal morbidity. Routine ultrasound scanning may be effective and useful as a screening for malformation. Its use for this purpose, however, should be made explicit and take into account the risk of false positive diagnosis in addition to ethical issues.

In another 1993 review covering 15,530 births the authors found “no significant differences in maternal outcomes”. The rates of induced abortion, amniocentesis, tests of fetal well-being, external version, induction, and cesarean section and the distribution of total hospital days were similar in the two groups. They concluded:

Screening ultrasonography resulted in no clinically significant benefit.

In the same year (1993), the World Health Organization (WHO) issued a letter reviewing the studies performed on routine ultrasound to date and concluded ²:

It is fair to say that at the moment the best research shows no benefit from routine ultrasound scanning and the real possibility of serious risk. …we urge you to reconsider all present policy with regard to routine ultrasound scanning during pregnancy, based on these important scientific papers.

Articles in this series:

• Natural childbirth I: is homebirth more dangerous than hospital birth?
• Natural childbirth IIa: is ultrasound necessary and effective during pregnancy?
• Natural childbirth IIb: ultrasound not as safe as commonly thought
• Natural childbirth III: why undisturbed birth?
• Natural childbirth IV: the hormones of birth
• Natural childbirth V: epidural side effects and risks
• Natural childbirth VI: Pitocin side effects and risks
• Natural childbirth VII: Cesarean risks and complications

What determines our health?

On this blog we’ve discussed a number of answers to that question. In fact, I just wrote a series called 9 Steps to Perfect Health in which I listed what I consider to be the most significant lifestyle factors contributing to health and disease.

Then we have the contribution of genes – the DNA we inherited and how it shapes our development and health. Chris Masterjohn is writing an excellent series on genetics over at his blog, The Daily Lipid.

But recent research suggests another powerful influence on lifelong health: your mother’s nutritional status during (and even before) her pregnancy. In fact, some researchers now believe the 9 months of pregnancy are the most consequential period of our lives, permanently influencing the wiring of the brain and the function of organs like the heart, liver and pancreas. They also suggest that the conditions we encounter in utero shape everything from our susceptibility to disease, to our appetite and metabolism, to our intelligence and temperament.

You’re only has healthy as your mother’s womb

The idea that the nutritional environment we encounter in the womb affects not only our health at birth and during infancy, but throughout the rest of our adult lives, has come to be known as the Developmental Origins of Health and Disease theory, or DOHaD (gotta love that acronym).

The theory was first proposed by British researcher David J. Barker in the 1980s to explain a seeming contradiction: as British prosperity increased, so did heart disease. Yet geographically, the highest rates of heart disease were found in the poorest places in Britain. Barker found that rather than smoking, dietary fat or some other lifestyle cause, the factor that was most predictive of whether an individual would develop premature heart disease (before the age of 65) was their weight at birth.

Barker found that infants carried to full term with birth weights between 8.5 and 9.5 pounds had a 45 percent lower risk of developing heart disease later in life than infants born at 5.5 pounds. (They also had a lower risk of stroke, a 70% lower risk of insulin resistance and a slightly lower risk of blood pressure later in life.) As the chart below demonstrates, the risk declined in a linear fashion between 5.5 and 9.5 pounds, but started to increase again as birth weight rose above 9.5 pounds.

How the first nine months shapes the rest of your life

Over the last 25 years, Barker’s original work has been reproduced and expanded. If you do a quick search on Pubmed.org for “developmental origins of disease”, you’ll find references to the fetal origins of cancer, heart disease, allergies, asthma, autoimmune disease, diabetes, obesity, mental illness and degenerative conditions like arthritis, osteoporosis, dementia and Alzheimer’s.

The following list is just a small sampling of the literature on the subject:

• The metabolic syndrome. In a 2011 paper, Bruce et al showed that the onset of metabolic syndrome is “increasingly likely following exposure to suboptimal nutrition during critical periods of development”.
• Heart disease & diabetes. In 2002, Barker, the father of the DOHaD hypothesis, published a paper suggesting that slow growth during fetal life and infancy – itself a consequence of poor maternal nutrition – predisposes individuals to coronary heart disease, type 2 diabetes and hypertension later in life.
• Breast cancer. Hilakivi-Clarke, et al . “Thus, maternal diet and environmental exposure might increase the risk of breast cancer by inducing permanent epigenetic changes in the fetus that alter the susceptibility to factors that can initiate breast cancer.”
• Polycystic ovary syndrome (PCOS). Dumesic et al 2007. This paper suggested that insulin resistance and resulting increases of testosterone during pregnancy promotes PCOS during adulthood.
• Obesity. Kalliomaki et al 2008. These researchers found that simply by studying the composition of the maternal gut flora (influenced by nutrition, medications, stress, etc.) they could predict which children will be overweight by age 7!

There are literally hundreds of similar papers in the literature, all pointing to the same conclusion: the nutritional environment in the womb has a significant effect on our health later in life.

Why does Mom’s diet play such a crucial role in determining our future health?

The idea that the nutritional, hormonal and metabolic environment provided by the mother permanently programs the structure and physiology of her offspring was established by Barker back in the 80s.

Essentially, it works like this. Like all living beings in their early lives, humans are able to adapt to their environment. If we couldn’t, we would die. There is a critical period early in life where that adaptation happens, and once that period passes, we become less “plastic” and able to adapt. Our programming is set.

For humans, that critical period when a system is plastic and sensitive to its environment occurs in utero. This makes perfect sense in evolutionary terms. It enables the production of genetic phenotypes that make us better matched to the environment we are likely find ourselves in after we’re born.

For example, if the mother’s nutritional status is poor during pregnancy, the fetus might develop metabolic adaptations that would allow it to store more calories (the “thrifty phenotype” hypothesis). This would have been a protective mechanism that could increase the chances of survival if that fetus was born into an environment where calories were scarce. G

Gluckman et al extended this concept of developmental plasticity by showing that fetal programming operates across the range from undernutrition to overnutrition with a U-shaped curve. This means that the future health of the baby will be affected when Mom gets either too little of the right nutrients or too much of the wrong ones.

Roseboom et al found that undernutrition during pregnancy affects different organs of the body and increases the risk of disease independent of birth weight. Other researchers have theorized that maternal diet may regulate blood flow to developing organs (i.e. to the brain vs. the liver) which in turn causes changes in fetal programming that affect body composition at birth and even later in life.

The nutritional conditions in the womb start before conception

We’ve now established that the nutritional environment of a mother’s womb affects her baby’s health not only at birth and during early infancy, but for the rest of his or her life. This leads us to the obvious conclusion that proper maternal nutrition is crucial for the lifelong health of her offspring.

But what determines the mother’s nutritional status during pregnancy? Certainly, the obvious answer is her diet and lifestyle after she has conceived. But I hope it’s also obvious that the mother’s diet in the months and even years leading up to conception is also important.

This is why traditional cultures have sacred fertility foods they feed to mothers-to-be and even fathers-to-be. These include nutrient dense foods like fish eggs, liver, bone marrow, egg yolks and other animal fats. For example, the Masai tribe in Africa only allowed couples to marry and become pregnant after spending several months drinking milk in the wet season when the grass is lush and the nutrient content of the milk is especially high.

Unfortunately this traditional wisdom has been largely lost in the modern world. The role of nutrition during pre-conception is scarcely even mentioned in the media or conventional medical settings. Yet as we’ve seen in this article, a mother’s diet prior to conception and during pregnancy may be one of the most important factors in determining the lifelong health of her baby.

Another problem is that many women are (understandably) confused about what constitutes proper nutrition during the pre-conception and pregnancy period. There’s so much contradictory information out there, and it can be difficult for the layperson to know what to believe and who to trust.

As many of you know, I’ve been teaching a seminar called Grow a Healthy Baby on nutrition for fertility, pregnancy and breastfeeding locally in the Bay Area for the past several months. I’m excited to announce that this material will soon be available as an online home study course. I’m shooting for mid-May as a launch date.

To learn more about the course and sign up to be notified when it becomes available, click here to join the mailing list. I’ll be making a special limited-time offer to people on this list, so be sure to sign up early if you’re interested in the course.

So far in this series we’ve looked at why fish is superior to plant-based sources of omega-3. We’ve examined the importance of reducing consumption of omega-6 fats. We’ve considered how much omega-3 is needed to support health and treat disease. And we’ve revealed that concerns about the safety of fish consumption have been overblown, and that eating fish regularly is not only safe, but incredibly beneficial.

In this article we’re going to compare fish with fish oil as a means of meeting our omega-3 needs, and for overall health and wellness. The comparison will be based on the following criteria: nutrient content, potency, absorption, cost and environmental impact.

Fish oil has become wildly popular in the last few years, as people increasingly understand the importance of omega-3 in the diet. However, part of the reason for fish oil’s popularity is related to concerns about the safety of eating whole fish – concerns that we now know are unfounded.

With this in mind, let’s see whether whole fish or fish oil are the best choice for most people.

Nutrient content

Fish: contain not only EPA and DHA, but also vitamin D, selenium, protein, co-factors and a more complete fatty acid profile than fish oil. Selenium, in particular, is important because it protects against mercury toxicity. Vitamin D protects against nearly every modern disease plaguing us today. A 6 oz. portion of wild salmon contains 1,700 IU of D, which is difficult to obtain in that amount from other dietary sources.

Fish oil: most oils contain only EPA and DHA, although salmon and cod liver oil also contain moderate amounts of vitamin D. Fish oil has a more limited fatty acid profile than whole fish, and doesn’t contain selenium.

Potency (levels of EPA & DHA)

Fish: a 6 oz. portion of wild salmon contains 883 mg of EPA and 1,111 mg of DHA. 2-3 servings a week of salmon, combined with a low intake on omega-6, would be adequate for most people.

Fish oil: this is where fish oil may have an advantage over fish. Because it is molecularly distilled and purified, fish oil can have high concentrations of DHA and EPA. 6 capsules of Jarrow Max DHA would provide 1.5g/day of DHA, a level that would be difficult to obtain from eating fish. You’d have to eat approximately 8.5 ounces of wild salmon every day to obtain that much DHA.

Absorption

Here’s where things get a bit tricky. I talked about potency above, and mentioned the levels of EPA and DHA in both fish and fish oil. However, those levels mean very little unless we consider how well they’re absorbed.

Several studies indicate that fish oil supplementation is not as effective as epidemiological evidence on the benefits of fish consumption suggest it would be. It appears that the presence of other fats in the fish activates processes required to absorb the EPA and DHA properly. This explains why the EPA and DHA are better absorbed from eating whole fish than from taking fish oil.

In one study comparing the effects of fish and fish oil, researchers found that levels of DHA after 6 weeks of salmon consumption were nine times higher than after fish oil administration.

The authors hypothesized that the configuration of fatty acids in whole fish is familiar to our body and thus easier to absorb. Conversely, the fish oil alone doesn’t adequately activate the process of fat absorption required to assimilate the fatty acids.

Another study confirmed this by demonstrating that fish oil is absorbed much better in the presence of a high-fat meal. They found that the content of n-3 fatty acids in the body tissues rose dramatically when the fish oil was taken along with 12g of olive oil.

We can draw two conclusions from these studies:

1. EPA, and especially DHA, is much better absorbed from fish than fish oil. The effect may be as great as nine-fold. This means that we would need nine times less DHA from fish to obtain the same amount of DHA from fish oil. Put another way, we’d need nine times more DHA from fish oil to obtain the same amount of DHA from fish. So, using the 6 oz. portion of salmon as an example, with 1.1g of DHA, we would need to take 9.9g of DHA from fish oil – roughly 36 capsules/day of the Jarrow Max DHA – to obtain the same amount of DHA we’d get from the salmon. That’s a lot of fish oil!
2. On the other hand, taking fish oil capsules with a high-fat meal can greatly improve their absorption, to the point where they may be on par with whole fish. (I say “may be” because the scientific literature is mixed on this.) This is likely due to the effect described above, where the presence of other fats activates the body’s fat absorption mechanisms.

Cost

This is also tricky to compare, since prices and availability of fish vary regionally. A straight comparison of the cost of DHA obtained from fish and fish oil also ignores other important factors, which we’ve already discussed above, such as the presence of other nutrients and the differences in absorption.

Let’s assume for the sake of comparison that fish oil is taken with a high-fat meal to improve absorption and that absorption rates of EPA and DHA are roughly similar between the two. Let’s assume that wild salmon is available for $13/lb. (I know it is much less in some areas, and much more in others).

Let’s assume also that we’re shooting for a daily intake of 500 mg of DHA.

To obtain this amount of DHA from salmon, you’d have to eat just over one pound per week (19 ounces). That would cost you $15.45.

To obtain this amount of DHA from Jarrow Max DHA, you’d have to take 2 capsules per day. Assuming you bought a bottle of 180 capsules from Vitacost for $14.70, you’d pay just $1.14 for the same amount of DHA.

However, you’d have to consider the following caveats:

1. It’s uncertain whether, even with a high fat meal, you’d be absorbing the same amount of DHA from the fish oil as you would from the salmon
2. The salmon has large amounts of protein, selenium, vitamin D and other fatty-acids and co-factors that the Jarrow fish oil doesn’t have
3. Other oily fish that are significantly cheaper than salmon, such as sardines and mackerel, are also very high in EPA and DHA.

Environmental impact

Overfishing and fish farming have already seriously damaged the health of marine ecosystems, and threaten to do even more damage if fish and fish oil consumption increases.

Much has been written about this elsewhere. Charles Clover’s The End of the Line: How Overfishing is Changing the World and What We Eat provides a particularly astute (and scary) analysis of the impacts of current methods of fishing on global ecosystems.

In short, I believe the most responsible choice we can make is to limit the fish we eat to those certified by groups like the Marine Stewardship Council (MSC).

However, even those groups are not infallible. Recently concerns have been raised over MSC’s decision to certify a salmon fishery in British Columbia where the salmon population is declining rapidly. Environmentalists and scientists have protested the decision, but the MSC seems to have moved ahead regardless.

Unfortunately it’s not a cut and dry issue, and those who are interested in eating fish harvested in a sustainable matter will have to do their own research and stay abreast of changing policies and practices.

In general, though, most environmentalists and scientists support the MSC certification. MSC has a list of fish they consider safe to eat on their website, which you can refer to.

MSC also has a certification label (pictured below) they provide to vendors of MSC-certified fish that you can look for when you’re shopping.

The sustainability of fish oil production is even more difficult to gauge. Some oils are produced as a byproduct of fish harvesting, and manufacturers claim that they are simply making use of something that would normally be discarded. While this is certainly better than harvesting fish solely for their oil, it still supports harmful fishing practices.

The safest bet is to only use fish oil that is made from fish that are certified by MSF or a similar organization, such as the Environmental Defense Fund. Vital Choice Wild Salmon Oil is one example, as is Jarrow Max DHA (which is made from anchovies and sardines, both of which are generally regarded as safe to eat from an environmental standpoint).

The verdict

The question of whether fish or fish oil is a better choice is complex and depends upon several different factors. These include whether DHA is needed for maintenance or therapeutic effect, access to sustainability caught wild fish, financial considerations, and the presence of other nutrients in fish.

For those who are generally healthy and want to stay that way, I think reducing omega-6 consumption and eating a moderate amount of oily fish (2-3 6 oz. portions per week) is the best choice. This will get you plenty of EPA & DHA along with high quality protein, selenium and vitamin D. If wild salmon is out of your price range, mackerel and sardines are both high in EPA and DHA and certified by the MSC as safe to eat.

For those who have a chronic, inflammatory condition such as cardiovascular disease or an autoimmune disorder, I would recommend a combination of whole fish (perhaps the same 2-3 6 oz. portions per week) along with a high quality fish oil. This ensures that you are getting the benefits of whole fish along with the added therapeutic effect of higher doses of DHA and EPA. Somewhere around 1.5g per day of DHA would be a good therapeutic dose, which would mean taking 1g/day of DHA in fish oil capsules in addition to the three 6 oz. portions of oily fish.

In the next and final article of this series, I’ll discuss the criteria for choosing a fish oil and make recommendations based on those criteria and clinical experience.

I just came across a website called Modern Paleo, put together by Diana Hsieh. It has a section called “modern paleo principles” with a list of 30 nutritional and lifestyle recommendations for staying healthy and avoiding disease.

If you’re looking for a good “blueprint” for health to follow, this is it. It’s one of the bests lists of this kind that I’ve seen. I agree with Diana on every point, with the exception of #30 (which is more about politics than nutrition). I also have some minor quibbles on #2/#6 (I think grains and legumes are okay in moderation when properly prepared/soaked, and I definitely think refined grains are worse than whole grains), #15 (although some nuts are high in omega-6, they are nutrient-dense whole foods with antioxidants to minimize oxidative damage), and #19 (I don’t recommend most commercial fish and cod liver oils, which are rancid, contain synthetic nutrients, or are not high enough in DHA/EPA to have a therapeutic effect).

I’m re-posting the first ten principles here with Diana’s permission. Visit this page on the Modern Paleo website to read the remaining 20 principles. Even better, Diana has included links to additional information for each principle that you can access by clicking on the “+/-” sign.

One last thing. As the saying goes, “don’t let the perfect be the enemy of the good.” Embrace the 80/20 rule with these principles. If you follow them 80% of the time, you’ll be on the fast track to vibrant health. An occasional ice cream or piece of bread isn’t going to kill you or reverse the positive effects of this approach. (Of course this isn’t true for those with true intolerances to dairy and gluten. In that case, 100% avoidance is the rule.)

Modern Paleo Principles: A Work-In-Progress

These principles are in a rough order of importance. If you’re overwhelmed by them, try working your way down the list slowly.

1. Eat real foods, prepared well. Prepare your own food as much as you can. Beware the junk ubiquitous in convenience and restaurant foods.
2. Don’t eat wheat, corn, rice, or other grains. If you choose to eat some grains, eat them sparingly and prepare them to minimize toxins, such as by sprouting and soaking. Wheat seems to be the worst of all the grains, while rice seems to be the most benign. Whole grains are not better than refined grains.
3. Don’t eat sweets: avoid sugar, corn syrup, agave nectar, honey, maple syrup, and artificial sweeteners. If you must have some sweetener for a dish, you might try a bit of stevia. With time, your tastes will adjust: ordinary sweets will taste cloying, but formerly bland vegetables will seem delightfully sweet.
4. Don’t eat modern oils derived from grains and seeds — such as canola oil, corn oil, or soy oil. Make your own mayonnaise and salad dressing. Don’t eat fried foods in restaurants: rancid vegetable oils are standard for frying. Avoid all hydrogenated fats; they contain damaging artificial transfats. Instead, use liberal amounts of animal fats — like butter, ghee, lard, and tallow — as well as unrefined coconut oil and olive oil. (Reserve your bacon grease: it’s delicious rendered lard!) Do not fear saturated fat: it’s healthy, including for your heart.
5. Don’t eat soy. Some fermented soy might be okay, if tolerated. However, all soy is goitrogenic and contains estrogen-mimicking hormones.
6. Don’t eat beans and other legumes. If you choose to eat some legumes, eat them sparingly and prepare them to minimize toxins, such as by soaking them.
7. Watch your ratio of omega-6 to omega-3 polyunsaturated fats, as well as your total omega-6 intake. Most people eat far too much omega-6, both absolutely and relatively. Today, the average ratio of omega-6 to omega-3 in Western diets is 17:1, but the ideal ratio looks to be between 2:1 and 1:4. To achieve that you’ll need to limit omega-6 intake by eliminating modern vegetable oils and eating high-omega-6 nuts sparingly. You’ll likely need to supplement with high omega-3 fish oil too.
8. Eat plenty of high-quality meat, preferably from pastured animals. Grass-fed meats have a better ratio of omega-6 to omega-3 polyunsaturated fats than grain-fed meats. Avoid meats treated with antibiotics and hormones, if feasible: the animals are likely treated better, and they taste better. Enjoy plenty of red meat. Try uncured bacon and other breakfast meats. They might not be any healthier, but they taste so much better!
9. Eat eggs, preferably from pastured chickens. Eggs enriched with omega-3s are a good option too. Prefer nutrient-dense egg yolks to nutrient-poor egg whites.
10. Eat fish and shellfish periodically, preferably caught wild rather than farm-raised.

Don’t forget to click here to read the remaining 20 principles!

Back in July I posted an article called Statins For Pregnant Women and Kids? criticizing a research study that actually recommended statins for pregnant women.

Well, it appears that even mainstream scientists are beginning to acknowledge the very real risks that statins present for pregnant mothers and fetuses.

Current clinical guidelines already recommend that women who are pregnant should stop taking statins but the advice is based on the knowledge that cholesterol is essential for normal fetal development.

But new research from The University of Manchester has shown that even water-soluble or ‘hydrophilic’ statins, such as pravastatin, can affect placental development leading to worse pregnancy outcomes.

According to Dr. Melissa Westwood, a Senior Lecturer in Endocrinology based at the Maternal and Fetal Health Research Centre at St. Mary’s Hospital, Manchester:

Fat-soluble statins like cerivastatin were already known to adversely affect the placenta, resulting in reducing growth. But the researchers also found that pravastatin – the water-soluble statin thought to be potentially compatible for use in pregnancy – had the same detrimental effect.

I’d like to bring your attention to two recently published studies which highlight the dangers of antidepressant drugs and maintaining low cholesterol levels.

Low Serum Cholesterol May Be Associated With Suicide Attempt History

I’ve written before about the association of low cholesterol with aggressive and violent behavior as well as an increased risk of suicide. A recent study published in the Journal of Clinical Psychiatry adds weight to the already considerable body of evidence suggesting that low cholesterol is dangerous to your health.

In this study ‘low cholesterol’ was defined as less than 160mg/dL (4.16 mmol/L). This level has been noted several times in the medical literature as a level below which suicide is more likely. And you should note that this level is well within what is considered ‘healthy’ by a cholesterol-lowering, drug pushing health industry.

This is consistent with studies showing that low blood cholesterol levels are associated with suicide and that cholesterol levels in certain areas of the brain are lower in those who commit suicide by violent means than in those who commit suicide by non-violent means.

Cholesterol is a health-promoting substance. It is a critical component of cell membranes, the precursor to all steroid hormones, a precursor to vitamin D, and the limiting factor that brain cells need to make connections with one another called synapses, making it essential to learning and memory.

If you understand the vital role cholesterol plays in health – especially in the brain – it’s not difficult to figure out why low cholesterol could increase the risk of suicide and violent behavior.

This is yet another reason to avoid cholesterol-lowering statin drugs. If you haven’t read it already, you might want to check out my post called Cholesterol Doesn’t Cause Heart Disease.

(J Clin Psychiatry October 21, 2008: e1-e8; pii: ej07m03866)

Two Antidepressants Taken During Pregnancy Linked To Heart Anomalies In Babies

In another disturbing study, researchers from Israel, Italy and Germany found that pregnant women taking two popular antidepressants, paroxetine (Paxil) and fluoxetine (Prozac), were three and four times more likely to give birth to children with heart problems.

Researchers have advised women taking the drugs to continue unless they are advised to stop by their doctor or consultant.

I’ve written extensively here about the risks of antidepressant drugs, especially for pregnant women. In my recent post Statins For Pregnant Women and Kids? I presented evidence that statin drugs can cause birth defects and changes in the brain that predispose the child to emotional problems later in life. Here’s a brief excerpt:

If you’re pregnant or considering getting pregnant, please – for the sake of your baby – speak to your psychiatrist or doctor about getting off antidepressant drugs before you conceive.

Statins for pregnant women?

Statin manufacturers, the sycophantic researchers they pay, and the shameless hucksters who sell them are always up to no good, but their recent attempts to market them to pregnant women are simply horrifying.

According to a recent news article published in Mail online, researchers from liverpool believe that taking statins during pregnancy might help women avoid caesarean sections by promoting more robust uterine contraction. They hope to begin human trials in three to five years.

Somehow, the author of this article failed to react with the shock and horror appropriate to the situation — which should be the same shock and horror with which we would react to the suggestion that pregnant women should take thalidomide to avoid morning sickness.

Back in 2004, a report in the New England Journal of Medicine showed that the use of statins in the first trimester of pregnancy was associated with birth defects, especially severe central nervous system defects and limb deformities. In fact, 20 out of 52 women exposed to statins gave birth to offspring with such defects, which represents a birth defect rate of 38 percent, nearly 20 times the background rate of birth defects!

Even before this report was published, researchers already knew that statins caused birth defects in animal experiments, and the FDA already required the drugs to carry a label warning pregnant women to stay away from them. The article linked to above stated the following:

“FDA took this action because it was recognized that fetal cholesterol synthesis was essential for development, and because animals given statins during pregnancy had offspring with a variety of birth defects,” [one of the study's authors] said.

Less than a year later, Merck and Johnson & Johnson jointly asked the FDA for permission to market an over-the-counter statin. One of the concerns about the proposal was the risk to pregnant women. USA Today reported:

The FDA classifies Mevacor and other statins as pregnancy category X, which means they are not supposed to be taken by pregnant women. Not only have category X drugs been linked to fetal abnormalities in animal or human studies, but the FDA also has declared that the benefits of taking them do not outweigh potential risks.

According to the same article, Merck made a disturbing admission:

“Of course, there will be women who take it off-label,” acknowledges Merck executive Edwin Hemwall, referring to the use of non-prescription Mevacor by women under 55.

And what could prompt women to use statins during pregnancy against recommendations? Certainly a news article declaring that statins might prevent the need for caesarean sections and their associated complications could prompt some women to do so.

So what ground-breaking research made these Liverpool researchers so confident that taking drugs associated with twenty times the normal rate of major birth defects during pregnancy might be a good idea that they put out a press release declaring this confidence to the public before any trials were even under way?

Well, according to the article:

Tests have already shown that raising levels of cholesterol interferes with womb tissue’s ability to contract.
Really. Raising levels of cholesterol. You might wonder how they accomplished that. Did they use cholesterol-raising drugs? I don’t know of any drugs that do that. Did they use egg yolks, or the dreaded dietary villain — gasp — saturated fats?

No, the story is quite different.

The apparent basis for this ridiculous statin cheerleading is a 2004 study published by researchers from the University of Liverpool in the American Journal of Physiology — Cell Physiology entitled “Increased cholesterol decreases uterine activity: functional effects of cholesterol alteration in pregnant rat myometrium.”

Rather than feeding anything to pregnant women or pregnant rats, the researchers took pregnant rats and killed them. So the first thing we can say is that statins might help you deliver a baby if your doctor kills you first.

Then they extracted the uterine tissue and either extracted cholesterol from it with a chemical solvent called methyl beta-cyclodextrin, or enriched it either with cholesterol mixed with this solvent or with LDL (which they didn’t measure for oxidation prior to use). Then they added drugs to induce contraction under either cholesterol-depleted or cholesterol-enriched conditions, and found that contraction was greater under cholesterol-depleted conditions.

So now we know that — wait, what is it we know?

Well, quite clearly, we don’t know anything that we can have any confidence has any physiological relevance at all. That is, except the fact that statins cause birth defects in animals, and they increase the rate of birth defects in humans by nearly twenty times, primarily by causing severe defects of the central nervous system and limb deformities.

To add to that, we also know that the vast majority of humans conceived with Smith-Lemli-Opitz Syndrome (SLOS), a genetic inability to synthesize enough cholesterol, die of spontaneous abortion in the first 16 weeks of gestation. Those who live long enough to be born suffer from mental retardation, autism, facial and skeletal malformations, visual dysfunctions and failure to thrive.

Statins for pregnant women? I don’t think so.

Article written by Chris Masterjohn

Statins for 8-year old children?

The American Academy of Pediatrics recently announced new recommendations for giving cholesterol-lowering drugs to children as young as eight years old. They also recommend giving low-fat milk to infants as young as one year old.

The New York Times published several articles on this, first announcing the recommendation the day the academy made it, then describing the backlash of saner doctors and other members of the public against it, and finally editorializing that while they were first “appalled” at the recommendation, after reading the report they were more dismayed at the state of our children’s health.

Concerning this frightful state of children’s health, the Times reported the following:

“We are in an epidemic,” said Dr. Jatinder Bhatia, a member of the academy’s nutrition committee who is a professor and chief of neonatology at the Medical College of Georgia in Augusta. “The risk of giving statins at a lower age is less than the benefit you’re going to get out of it.”

Dr. Bhatia said that although there was not “a whole lot” of data on pediatric use of cholesterol-lowering drugs, recent research showed that the drugs were generally safe for children.

An epidemic of what? High cholesterol? Not according to the academy’s report, which states that cholesterol levels in children declined between 1966 and 1994 and stayed the same between 1994 and 2000.

No, we are in an epidemic of obesity. As the Times reported:

But proponents say there is growing evidence that the first signs of heart disease show up in childhood, and with 30 percent of the nation’s children overweight or obese, many doctors fear that a rash of early heart attacks and diabetes is on the horizon as these children grow up.

Is there any evidence that statins lead to weight loss? If there is, I am not aware of it.

The point is immaterial, because the academy doesn’t claim to have any evidence for its position in the first place. For example, its report states the following:

Also, data supporting a particular level of childhood cholesterol that predicts risk of adult CVD do not exist, which makes the prospect of a firm evidence-based recommendation for cholesterol screening for children elusive.
And further down:

It is difficult to develop an evidence-based approach for the specific age at which pharmacologic treatment should be implemented. . . . It is not known whether there is an age at which development of the atherosclerotic process is accelerated.

In other words, they don’t know what level of cholesterol is risky and at what age it starts posing a risk, but they will nevertheless assume that there is some level that does start to pose a risk at some age and they will thus have to make a guess just what that level and what that age is.

The report discusses evidence that the “metabolic syndrome” and the “recent epidemic of childhood obesity” are tied to the risk of diabetes and heart disease and evidence that even modest weight loss at a level of five to seven percent is sufficient to prevent diabetes. Yet somehow instead of making a recommendation about how to more effectively lose weight the authors derive from this data a much less logical but much more profitable conclusion that 8-year-olds should be put on statins.

As to the recommendation to feed infants low-fat milk, the Times reported the following:

The academy also now recommends giving children low-fat milk after 12 months if a doctor is concerned about future weight problems. Although children need fat for brain development, the group says that because children often consume so much fat, low-fat milk is now appropriate.

This is rather remarkable, because the academy attributed the drop in childhood cholesterol levels to the successes of the anti-fat, anti-cholesterol campaign that began in the 1950s. But now children no longer need milkfat because they are getting plenty of fat. Well which is it? Are they getting more fat now or less fat?

Of course milkfat is also a source of choline, along with liver and egg yolks, which is essential to brain development.

But even this misses the point. Cholesterol is essential to brain development!

One of the first articles I added to my section on the functions of cholesterol was an article entitled “Learning, Your Memory, and Cholesterol.” It discusses the evidence uncovered eight years ago that cholesterol is the limiting factor for the formation of synapses, which are the connections between neurons that allow learning and memory to take place.

Lowering brain levels of cholesterol can be detrimental at any age beacause of this, but the consequences for children — whose brains are still developing at a much more rapid rate — could be much more dire.

No doubt, most researchers and medical doctors mean well and are honestly trying to help our children. But surely someone in these drug companies must know that cholesterol is necessary for brain development, and that cholesterol-lowering drugs reduce mental performance in adults. Surely they must know that if we raise our next generation of children on statins during the critical periods of brain development, we may raise a whole generation with compromised intelligence.

And if that’s the case, are they trying to dumb us down? Sometimes it seems like that’s the case.

Article written by Chris Masterjohn

This week I’d like to bring your attention to three articles I came across on the web which illustrate the utter madness of mainstream medicine and nutrition.

The first article, “Beware of New Media Brainwashing About High Fructose Corn Syrup“, appeared on Mercola.com, a health advocacy site run by Dr. Joseph Mercola which I recommend. I agree with Dr. Mercola on most things, and even when we don’t agree the differences are relatively minor.

In his article Mercola warns consumers that The Corn Refiners Association is spending $20 to $30 million dollars on an advertising campaign to “rehabilitate” the reputation of high fructose corn syrup (HFCS), claiming that the product is “no worse for you than sugar.”

HFCS is now the #1 source of calories for children in the U.S., a staggering fact when research has clearly linked HFCS to obesity, diabetes, metabolic syndrome, high triglycerides, liver disease and more. On top of that, HFCS is almost always made with genetically modified corn.

Head on over to Mercola.com to read the rest of the article and learn why you and your children should be avoiding HFCS as much as possible. HFCS is found primarily in processed foods (in everything from hamburger buns to soda), so if you follow my general recommendation of eating a whole-foods diet you should have no trouble avoiding it.

The second article, “8-Year-Olds on Statins? A New Plan Quickly Bites Back“, was published in the New York Times on July 8. It describes new guidelines issued by the American Academy of Pediatrics recommending that statin drugs be prescribed to kids as young as 8 years old!

While some doctors applauded the idea (which is incomprehensible to me), others were “incredulous”. Why are they incredulous? Because there is absolutely no evidence suggesting that treating children with statins will prevent heart attacks or reduce mortality from heart disease. Furthermore, there are no data on the possible side effects from taking statins for 40 or 50 years. Since statins have caused cancer in several animal studies, there is no reason to assume that this is not a risk in humans – especially with such long-term use of the drugs.

If you’re not familiar with the dangers of statin drugs, I suggest you read my recent article “The Truth About Statin Drugs“. Not only are statins nowhere near as effective as claimed, they have serious adverse effects and risks – including death.

What’s more, statins have been neither studied nor approved for use with children. In other words, the American Pediatric Association wants to perform an uncontrolled experiment with statin drugs and our children. This is completely unacceptable in light of what we already know about these drugs.

This is yet another obvious example of how the massive conflicts of interest in the medical field, which I described in a previous article, cloud the judgment of otherwise well-meaning physicians and health organizations.

Head over to the New York Times to read the rest of the article.

The third article, “Popular Fish, Tilapia, Contains Potentially Dangerous Fatty Acid Combination” which appeared on ScienceDaily.com, revealed that farm-raised tilapia has very low levels of beneficial omega-3 fatty acids and, even worse, very high levels of omega-6 fatty acids.

This is particularly troublesome because tilapia has become one of the most highly consumed fish in the U.S. (mostly due to its low price), and that trend is expected to continue through 2010.

Researchers have found that tilapia has higher levels of omega-6 fatty acids than doughnuts. That’s scary.

The health risks of excessive amounts of omega-6 fatty acids in the diet are well established. In short, they are significant contributors to both inflammation and oxidative damage in the body. Inflammation and oxidative damage are major risk factors for heart disease, diabetes, cancer and many other diseases.

Wild-caught oily fish, on the other hand, contain a favorable ratio of omega-3 to omega-6 fatty acids and may actually protect against inflammation and oxidative damage?

So what’s the problem with tilapia, you ask? The problem is that they are raised on a “fish farm” where they are fed inexpensive corn-based feeds which contain short chain omega-6 fatty acids that the fish convert and store in their tissues. While this practice has kept the price of tilapia low, it has also transformed it into a toxic food.

Repeat after me: fish don’t eat corn. Fish don’t eat corn. Fish don’t eat corn.

(Cows don’t normally eat chicken parts, gummi bears and garbage, either; but they do in commercial feedlots where most of the meat in the U.S. is produced. I’ll save that for another day, though.)

What all of these articles share in common is 1) further evidence of the rampant conflicts of interest in our medical care system, 2) the complete lack of an objective, independent regulatory body that can protect consumers from the malfeasance of Big Pharma and Big Agrobusiness, 3) the general departure from common sense and traditional wisdom when it comes to health care and nutrition.

It’s absolute madness.

In a recent post, I discussed the consequences of the massive conflicts of interest that exist between researchers, doctors and the pharmaceutical industry in the U.S. and abroad.

On June 8th the New York Times published an article underscoring these consequences and illuminating the risks that inevitably come with financial ties between researchers and drug companies.

The article revealed that Dr. Joseph Biederman, a world-renowned child psychiatrist at Harvard, accepted at least $1.6 million in consulting fees from drug makers from 2000 to 2007 but did not disclose any of this income to university officials. By failing to report this income, Dr. Biederman and colleagues may have violated both federal and university research rules designed to prevent conflicts of interest.

Dr. Biederman is one of the most influential researchers in child psychiatry. Although many of his studies are small and often financed by pharmaceutical companies, his work has nevertheless directly contributed to a controversial 40-fold increase from 1994 to 2003 in the diagnosis of pediatric bipolar disorder and a concurrent rise in the use of powerful antipsychotic medicines in children.

We know from my previous post that it has been shown that studies funded by pharmaceutical companies are more likely to show positive results for the drug. We also know that the veracity of clinical trials which are the basis of approval of new drugs by the FDA has been called into question in recent studies because of three major flaws: conflicts of interest on the part of investigators (like Biederman); inappropriate involvement of research sponsors (drug companies) in study design and management; and publication bias in disseminating results (if a study has negative results, the drug company doesn’t publish it).

When a researcher like Dr. Biederman is paid millions by a drug company to study it’s product, we must wonder whether we can expect his work to be objective and accurate. But when that researcher repeatedly lies about the money he received, the integrity of his work should be in serious doubt.

In one revealing example, Dr. Biederman reported no income from Johnson & Johnson for 2001 in a disclosure report filed with Harvard University. When asked to check again, he said he received $3,500. But Johnson & Johnson told Congressional investigators that Mr. Biederman was paid $58,169 in 2001.

The consulting arrangements of Dr. Biederman’s entire research group at Harvard were already controversial because of the researcher’s advocacy of unapproved (“off-label”) uses of psychiatric medicines in children. Dr. Biederman and his colleagues have promoted the aggressive diagnosis and treatment of childhood bipolar disorder with antipsychotic drugs – although these drugs have never been approved for such use. In fact, neuroleptic drugs have not been approved for use in children at all.

As a result of Dr. Biederman’s promotion of both the diagnosis and treatment for childhood bipolar disorder, antipsychotic drug use in children has exploded. Roughly half a million children and teenagers were given at least one prescription for an antipsychotic in 2007, including 20,500 under 6 years of age, according to Medco Health Solutions, a pharmacy benefit manager.

The dramatic increase in antipsychotic prescriptions in children has occurred despite the lack of evidence that these medication improve children’s lives over time. On the contrary, it is well known that children are susceptible to the weight gain and metabolic problems caused by the drugs. Children typically gain twice as much weight in the first six months on atypical neuroleptic drugs (risperidone, olanzapine, etc.) as they should through normal growth, adding an average of 2 to 3 inches to their waistline. This is mostly abdominal fat, which also increases their risk of diabetes and heart disease.

There is also some evidence which suggests that these drugs may cause permanent changes to the structure and function of the brain (Breggin 1997). In other words, they cause brain damage.

The research of Dr. Biederman’s group, which has served as the basis for the rise in bipolar diagnoses and antipsychotic use in children, has been widely criticized by other psychiatrists and researchers.

The studies published by Dr. Biederman’s group were so small and “loosely” designed that they were largely inconclusive. In some studies testing antipsychotic drugs, the group defined improvement as a decline of 30 percent or more on a scale called the Young Mania Rating Scale, which is well below the 50 percent change that most researchers use as the standard.

Controlling for bias in these types of studies is particularly important, given that the scale is subjective and depends on reports from physicians, parents and children.

More broadly, psychiatrists have said that revelations of undisclosed payments from drug makers to leading researchers are especially damaging for psychiatry.

“The price we pay for these kinds of revelations is credibility, and we just can’t afford to lose any more of that in this field,” said Dr. E. Fuller Torrey, executive director of the Stanley Medical Research Institute, which finances psychiatric studies. “In the area of child psychiatry in particular, we know much less than we should, and we desperately need research that is not influenced by industry money.”

I couldn’t have said it better myself.

Although widely promoted as a health food, hundreds of studies link modern processed soy to malnutrition, digestive problems, thyroid dysfunction, cognitive decline, reproductive disorders, immune system breakdown, and even heart disease and cancer. How could soy be linked to all this disease? Because the soybean contains many naturally occurring toxins. All legumes contain toxins but the problem with soy is that the toxins are found in very high levels and are resistant to the traditional ways of getting rid of them.

Long, slow fermentation (as in the traditional production of miso, tempeh and soy sauce) gets rid of the phytic acid and other digestive inhibitors but not the phytoestrogens in soy.

Myths About Isoflavones

One of the most common myths is that soy estrogens (isoflavones) are beneficial for your health. Isoflavones are the estrogen-like compounds occurring naturally in soy foods. They act as the plant’s natural pesticides, causing insects to become sterile. Research has shown that isoflavones can prevent ovulation and stimulate the growth of cancer cells. As little as 38 mg isoflavones per day (less than the amount found in 1 cup of soy milk) can result in hypothyroidism with symptoms of lethargy, constipation, weight gain and fatigue. The isoflavones in soy have been shown to cause reproductive problems, infertility, thyroid disease and liver disease in mice, rats, cheetahs, sturgeon, quail, sheep, pigs and marmoset monkeys.

Traditional Versus Modern Soy Foods

It is important to distinguish between traditional and modern soy foods. In Asia, traditional soy foods were consumed in small amounts, usually as a fermented condiment. Traditional fermented soy foods include miso, soy sauce, tempeh and natto. Tofu was prepared by a precipitation process that gets rid of some of the anti-nutrients, and tofu was often then fermented. Tofu was usually consumed in small amounts in fish broth, which provided lots of compensating minerals and compounds that support thyroid function.

Soymilk underwent a very long preparation process to get rid of anti-nutrients and it was consumed with shrimp or egg yolk, ingredients that helped compensate for the many anti-nutrients that remained. Mostly a food for the elderly, it was sometimes given to nursing mothers but never to growing children.

Problems with Soy Protein Isolate

Modern soy foods are very different. Most are made with soy protein isolate (SPI), which is a protein-rich powder extracted by an industrial process from the waste product of soy oil manufacturing. It is the industry’s way of making a profit on a waste product. The industry spent over 30 years and billions of dollars developing SPI.

Soy Protein Isolate is produced at very high temperatures and pressures. This processing does get rid of some of the anti-nutrients in soybeans, but unfortunately many of the proteins are denatured in the process, including lysine. That is why growing animals fed soy must be given a lysine supplement. In feeding studies, SPI caused many deficiencies in rats. That soy causes deficiencies in B12 and zinc is widely recognized; but the range of deficiencies was surprising.

Although SPI is added to many foods, it was never granted GRAS status, meaning “Generally Recognized as Safe”. The FDA only granted GRAS status to SPI for use as a binder in cardboard boxes. During the processing of soy, many additional toxins are formed, including nitrates (which are carcinogens) and a toxin called lysinoalanine. It was concerns about lysinoalanine in SPI that led the FDA to deny GRAS status for SPI as a food additive.

In spite of all these problems, SPI is the basic ingredient of soy infant formula and the FDA even allows a health claim for foods containing 6.25 grams SPI per serving.

The Dangers of Soy Infant Formula

Infants on soy formula can take in dangerously high levels of soy isoflavones. On a body weight basis, this can mean ten times the level that can cause thyroid suppression in adults after three months, and eight times the level that can cause hormonal changes in adults after just one month.

According to a Swiss report adult women consuming 100 mg isoflavones (about 2 cups of soy milk, or 1 cup of cooked mature soybeans) provide the estrogenic equivalent of a contraceptive pill.

This means for a baby that weighs 6 kg (or just over 13 pounds), 10 mg provides the estrogenic equivalent of a contraceptive pill. Thus, the average amount of soy-based formula taken in by a child provides the estrogenic equivalent of at least four birth control pills. Because babies are more vulnerable than adults to the effects of dietary estrogens, the effects could actually be much greater than that of four birth control pills.

Hence the statement, “Babies on soy formula receive the estrogenic equivalent of at least five birth control pills per day.”

Homemade Baby Formula

For adopted infants, or as a solution for mothers who aren’t physically able to breastfeed or who aren’t able to produce enough milk, we’d like parents to know that there are nutrient dense, homemade Baby Formula Recipes in the book Nourishing Traditions which have been used with great success by parents all over the world since 1995!

The Healthy Skeptic reader Jessica wrote in with this topic suggestion:

“I like the “what to feed children” idea. But it has to be food they will actually EAT.”

The question of how to nourish our children so they develop into healthy adults is one of the most important questions we can ask. Tragically, the answers that the medical mainstream has come up with have contributed to unprecedented epidemics of childhood disease and endangered the health and well-being of our children.

The numbers of overweight and obese children worldwide are expected to climb dramatically by 2010, according to a study by Youfa Wang, PhD, MD at the Johns Hopkins Bloomberg School of Public Health. By the end of the decade, 46 percent of children in North and South America are projected to be overweight and 15 percent will be obese. It’s been assumed that U.S. life expectancy would rise indefinitely, but a new data analysis which was published as a special report in the March 17, 2005 issue of New England Journal of Medicine suggests that this trend is about to reverse itself – due to the rapid rise in obesity, especially among children.

Increasing numbers of children are being treated for depression, according to a 2004 study in the British Journal of Medicine. A 1999 report in California from the state’s Department of Developmental Services found that autism had increased by 273 percent from 1987 to 1998. Current estimates for the incidence of autism are as high as 1 in 120. A national review by The Advocacy Institute in 2002 revealed that learning disabilities in children increased by 30 percent from 1990 to 2000.

These studies show that our children are more obese, more depressed, and have more learning disabilities and behavioral problems than ever before. What could be the cause of such a dramatic change?

Although each of these diseases is complex and multifactorial, it is safe to say that diet and nutrition play a significant role in all of them. For example, consider the key nutrients for brain development in children:

Many parents probably know that these nutrients aren’t found in the refined carbohydrates, vegetable oils and sugars which form the bedrock of the standard American diet. Yet many parents may be unaware that even foods widely assumed to be nutritional – including packaged foods commonly described as “organic”, “natural” or “fortified” – are themselves highly processed and stripped of nutritional value, and little better than their “non-organic” alternatives.

So what should we be feeding our children to ensure healthy growth and development? The following “First Steps” recommended by children’s health advocacy group Nourishing Our Children will get you started:

In contrast to the bland, unsatisfying (and dangerous) low-fat diet recommended by medical authorities, kids naturally love the foods in a nutrient-dense, whole foods diet. However, it is true that if they’ve been on a diet high in sugar and refined carbohydrates for a long time, there will be an adjustment period as they transition away from those highly processed foods.

My suggestion is to take one item on the list above at a time, and be gentle with yourself. It may take a while longer that way to get to where you want to be, but it’s worth the effort! Some of the changes will be more difficult than others. For example, most children (and adults) prefer the taste of saturated fats like butter, cream and whole-fat dairy to low-fat alternatives such as vegetable oil and skim milk – but may not yet have acquired a taste for cod liver oil!

I’ve provided links to some articles below with some helpful ideas on how to encourage even the most finicky eaters to enjoy nutrient-dense foods and some ideas for quick and healthy brown-bag lunch suggestions for parents.

Recommended links

• Articles on children’s health – Weston A. Price Foundation
• Feeding Our Children, by Thomas Cowan, M.D.
• Taking the Icky out of Picky Eaters
• Foods to Tantalize Toddlers and Preschoolers
• Packing the Perfect Lunch Box
• Nourishing Our Children – children’s health advocacy group

Exposure to sunlight prevents melanoma.

Yes, you did read that correctly.

Two independent studies published in the Feb. 2005 issue of the prestigious Journal of the National Cancer Institute (JNCI) squarely contradict the popular myth that UV light causes melanoma.

The first study evaluated the hypothesis that UV radiation increases your risk of developing lymphoma – a hypothesis that had become widely accepted in the 1990s and early 2000s. After studying nearly 7,000 subjects, the authors concluded that the opposite is actually true: increased sun exposure reduces the risk of non-Hodgkin’s lymphoma (NHL) by up to 40%. What’s more, the reduction in risk was dose-related, which means that the more sun exposure someone got, the lower their risk of cancer was.

The second study looked at the link between sun exposure and the chances of surviving melanoma, which is the deadliest form of skin cancer. Guess what? The researchers concluded that increased sun exposure decreases the chance of dying from skin cancer by approximately 50%.

At this point you might be scratching your head and wondering how this could possibly be true, in light of what we’ve been told all these years about the relationship between sunlight and skin cancer. Let’s take a closer look at what explains this phenomenon, and why you likely haven’t heard about it on the news.

Clarification

An editorial published in the same issue of JNCI begins with this statement:

“Solar radiation is a well-established skin carcinogen, responsible for more cancers worldwide than any other single agent.”

This is true. But what the authors neglect to mention is that the type of cancer they are referring to is not melanoma but other types of cancer. Melanoma is the most serious form of skin cancer because it is malignant and can metastasize (spread) to other areas of the body, often leading to death.

But 90 percent of skin cancers are not melanomas. Rather, the most common forms are basal and squamous cell carcinomas, which are often benign and easily cured by simple outpatient surgery. These non-malignant forms of skin cancer are indeed caused by solar radiation (at least according to current research). Melanomas, however, are most likely caused by lack of sunlight or excess exposure to artificial light!

The editorial mentioned two other very important facts that you aren’t likely to hear about from mainstream media sources: that melanoma is normally found in areas of the body that are not typically exposed to sunlight at all (use your imagination), and that vitamin D may be important in preventing melanoma.

Here’s what they actually had to say:

Umm, like, we already knew that.

The role of Vitamin D

It has been known for several years that sun exposure might have a beneficial effect on certain cancers. A 1999 publication of the National Institute of Health (NIH) entitled Atlas of Cancer Mortality in the United States revealed that among caucasians in the United States, cancer mortality for several prominent cancers, including cancer of the breast, prostate and colon, shows a striking latitudinal gradient. Specifically, people living in northern states have much higher rates of these cancers than those residing in the southern states.

The reason for this? Northern states get a whole lot less sunshine than southern states.

As early as 1990 it was proposed that vitamin D, which is synthesized in the skin upon exposure to UV light, might be the agent that accounts for these geographical patterns. (Garland et al. 1990) Less exposure to sunshine means less production of vitamin D. It is known that calcitriol, the active form of vitamin D3, has multiple cellular affects that could confer protection against cancer. The ability to convert the precursor to vitamin D to the active form of D3 (calcitriol) is greatly reduced at northern latitudes, and populations living far from the equator are at increased risk of vitamin D deficiency during the winter months. (Tangpricha et al. 2002)

Even more significant may be the observation that patients with malignant melanoma exhibit low levels of vitamin D3 in their blood, and that others have a problem with the receptor for vitamin D. (Hutchinson et al. 2000; Green et al. 1983) The incidence of melanoma of the skin on sites of the body intermittently exposed to sunlight is reduced among outdoor workers compared with indoor workers. (Elwood et al. 1985)

All of this points to a protective role for vitamin D against cancer in general, and melanoma in particular. But the final nail in the coffin of the “sunlight causes melanoma” hypothesis is this:

A comprehensive review of research studies from 1966 through 2003 failed to show any association between melanoma and sunscreen use! (Dennis et al. 2003)

Say what? Sunscreen doesn’t prevent skin cancer, that’s what.

Does sunscreen contribute to skin cancer?

One thing sunlight does cause is an injury to the inner layer of the skin (called the “dermis”), which leads to a wrinkling of the outer layer (called the “epidermis”). This phenomenon, which happens naturally with age but is accelerated by sun exposure, is called “solar elastosis”, or SE.

Sounds like a bad thing, right? But when researchers at the University of New Mexico studied melanoma, they found a marked decrease in the disease in patients with SE. (Berwick et al. 2005). To put it simply: more sun exposure equals lower risk of melanoma. For patients who already had melanoma, the subsequent death rate from the disease was approximately one-half as high in the group of patients with signs of SE.

I’ll give you a minute to finish cursing the “medical authorities” that have been admonishing us to slather ourselves and our children with sunscreen for decades in order to “prevent skin cancer”. As it turns out, if we followed this advice (and why wouldn’t we have? It sounded logical…) we have actually increased our chances and our children’s chances of developing not just skin cancer, but other cancers as well.

I’m sorry to scare you like that, but I feel I must in order to make this point as clearly as I can:

As we have already discussed, sunlight is a major source of vitamin D. Insufficient levels of vitamin D can result in osteoporosis, autoimmune diseases and rheumatoid arthritis – among other equally unpleasant and life-threatening conditions. When you put on those high-SPF sunscreens, not only are you increasing your risk for melanoma, you are increasing your risk of developing all of the conditions that can arise from vitamin D deficiency because you are blocking your body’s ability to synthesize vitamin D.

And while it is possible to obtain vitamin D from food, it is only present in large amounts in certain kinds of seafood – which many people do not consume regularly. The highest sources for vitamin D in food are anglerfish liver, cow’s blood (I’m not joking) and high-vitamin cod liver oil (HVCLO). It is also present in more modest amounts in chum salmon, Pacific marlin, herring, bluefin tuna, duck eggs, trout, eel, mackerel and salmon.

I’m going to go out on a limb and guess that most Americans aren’t eating these foods on a regular basis. The lack of adequate intake of vitamin D in the diet, combined with habitual use of high-SPF sunscreen and/or lack of exposure to the sun is a perfect recipe for increasing the risk of cancer for children and adults alike.

But you will not hear the sunscreen manufacturers telling you to stop using their product, and you probably won’t hear it from dermatologists in the field who have a reputation (and a history of telling people to wear sunscreen) to protect. They’ll tell you that sunburn is an important factor in melanoma formation since that’s really all they have left in terms of support for selling sunscreen. What they neglect to mention is that 1) millions of people get sunburned every year but very few develop melanoma, and more importantly, 2) if melanoma does appear, it’s most likely to appear in areas not exposed to the sun.

Nevertheless, it’s still probably a good idea to avoid getting sunburned – especially on a regular basis. But it is not a good idea to wear sunscreen, nor is it a good idea to avoid sun exposure.

The idea that sunlight causes cancer and sunscreen prevents it is another mainstream myth that has no support in the scientific literature. Just like the idea that cholesterol causes heart disease, eating fat makes you fat, and fluoride is good for your teeth. (If you still believe any of those statements, check my archives and sign up for my free email digest!)

Before closing, I must mention (briefly) the issue of vitamin D toxicity. Vitamin D is widely considered to be the most toxic of all vitamins, and dire warnings are often issued to avoid excess sun exposure and vitamin D in the diet on that basis. The discussion of vitamin D toxicity has failed to take into account the interaction between vitamins A, D and K. Several lines of evidence suggest that vitamin D toxicity actually results from a relative deficiency of vitamins A and K.
So, the solution is not to avoid sun exposure or sources of vitamin D in the diet. Rather, it ensure adequate vitamin D intake (through sunlight and food) and to increase the intake (through diet and/or supplements) of vitamins A & K. Stay tuned for a future post on the interaction between vitamins A, D & K and their relevance to human health.

In the meantime, this is what I recommend for protecting against cancer and both deficiency and toxicity of vitamin D:

As always, leave a comment or contact me with questions!

(Excerpted from the Weston A. Price foundation Journal: Caustic Commentary – Summer 2007)

Full-fat milk has pretty much disappeared from the public schools—not just in the US, but also in New Zealand, Australia and the UK. In most schools, children have a choice of watery reduced-fat milk or sugar-laden chocolate milk, based on the misconception that the butterfat in whole milk will cause heart disease later in life. So it’s a bit embarrassing when a study comes along showing that whole-fat milk products may help women conceive. Over a period of eight years, Jorge E Chavarro of the Harvard School of Public Health in Boston assessed the diets of 18,555 married women without a history of infertility who attempted to get pregnant or became pregnant. During the study, 2165 women were examined medically for infertility and 438 were found to be infertile due to lack of ovulation. The researchers found that women who ate two or more servings of lowfat dairy foods per day, particularly skim milk and yogurt, increased their risk of ovulation-related infertility by more than 85 percent compared with women who ate less than one serving of lowfat dairy food per week (Human Reproduction, online February 28, 2007). Chavarro advises women wanting to conceive to consume high-fat dairy foods like whole milk and ice cream, “while at the same time maintaining their normal calorie intake and limiting their overall intake of saturated fats in order to maintain good general health.” Once a woman becomes pregnant, says Chavarro, “she should probably switch back to lowfat dairy foods.” No one has looked at the effect on fertility of lowfat dairy for the developing fetus and for growing school children. Odds are that infertility due to life-long fat starvation will not be so easily reversed by a temporary return to high-fat dairy foods.

And Fatter?

Will lowfat milk served in schools not only make our children infertile, but also fatter? That’s the conclusion from a 2006 Swedish study which looked at 230 families in Goteborg, Sweden. Almost all of the children were breastfed until five months and 85 percent had parents who were university educated. Seventeen percent were classified as overweight, and a higher body mass index (BMI) was associated with a lower fat intake—and those on lower fat diets consumed more sugar. A lower fat intake was also associated with high insulin resistance (www.ub.gu.se/sok/dissdatabas/detaljvy.xml?id=6979).

Whole Fat Milk, Lower Weight Gain

In yet another defeat for the lowfat, you-must-suffer-to-lose-weight school of thought, a Swedish study has found that women who regularly consume at least one serving of full-fat dairy every day gained about 30 percent less weight than women who didn’t. The researchers, from the Karolinska Institute in Stockholm, looked at the intake of whole, sour, medium- and lowfat milk, as well as cheese and butter for 19,352 Swedish women aged 40-55 years at the start of the study. The researchers report that a regular and constant intake of whole milk, sour milk and cheese was significantly and inversely associated with weight gain (that is, those consuming whole-milk products did not gain weight), while the other intake groups were not. A constant intake of at least one daily serving of whole and sour milk was associated with 15 percent less weight gain, while cheese was associated with 30 percent less weight gain (American Journal of Clinical Nutrition, 2007;84(6):1481-1488). This wonderful scientific news has not inspired WebMD to remove their guidelines to eating “fabulous foreign foods.” The trick, they say, is to avoid dishes made with coconut milk in Thai restaurants; ghee, beef and lamb in Indian restaurants; and cream soups, cream sauces, béarnaise, creamy dressings, pâté, fatty meats, duck and sausages in French restaurants (onhealth.webmd.com). In other words, enjoy your meal out but not too much.