A: Vaginal atrophy and/or dryness is usually a consequence of a drop in estrogen. True vaginal atrophy – where vaginal tissue deteriorates drastically – is rare. It’s more likely that what you’re experiencing is vaginal dryness, and not only menopausal women suffer this. Estrogen production may drop while breastfeeding; douching, and yeast and other vaginal infections can also result in chronic vaginal dryness.

You are right that there has been little research into this problem as an isolated symptom. When mentioned, it‘s usually part of a catalogue of menopausal symptoms that have either improved or not with a particular drug or remedy.

After menopause as hormone levels change, the vagina can become thinner and narrower, and its natural secretions can decline. But a dry vagina is not a given in menopause. Some women have thinning of vaginal tissues but no dryness at all, while others have perfectly normal vaginal tissues, yet complain of dryness.

Although we don’t recommend reckless supplementation with phytoestrogens, this may be one case where soy phytoestrogens may be beneficial, though there are no data on which type of soy isoflavone is best for this condition. Each type has a unique impact on estrogen-sensitive tissues, and the various types of soy may have very different effects on the lower genital tract (J Clin Endocrinol Metab, 1995; 80: 1685-90; Maturitas, 1995; 21: 189-95). You may need to experiment to find the supplement best for you.

Black cohosh has been shown to benefit a range of menopausal symptoms, including vaginal dryness. Side-effects are few, but include occasional stomach upset, but the herb’s long-term effects have not been studied. It may lower your blood pressure, so don’t take it if you’re already taking an antihypertensive.

According to some herbalists, dandelion and oat-straw tea (rich in plant estrogens) can help restore normal vaginal lubrication.

You could also try using a simple, non-irritating, non-drying soap when washing. At night, wear a nightgown or long tee-shirt that allows air to circulate around your vagina. Avoid alcohol, caffeine and the antihistamines found in many cold remedies as all can dry the mucous membranes.

Staying sexually active to exercise the vaginal muscle is often advised, but seems to ignore the fact that a dry vagina can make sex painful. If you wish to maintain vaginal muscle tone, try integrating Kegel exercises – tightening and releasing the muscles around the vagina and anus several times in succession – into your daily routine. These exercises strengthen the pelvic floor muscles, improve sexual satisfaction and can help women of any age with urinary incontinence.

Keep you adrenals healthy since these glands continue to produce small amounts of estrogen. High levels of both vitamin C (at least 1000 mg daily) and pantothenic acid (50-300 mg daily) may be useful in supporting adrenal function. One study showed that vitamin E supplements can produce positive changes in the blood vessels of the vagina after just one month (J Obstet Gynaecol Br Emp, 1942; 49: 482).

You may need to use a personal lubricant until you find the remedy that works for you. Some women find a water-based lubricant such as KY Jelly or Replens helps to alleviate the problems associated with vaginal dryness. Mineral oil-based products, such as petroleum jelly and baby oil, should not be used because they tend to coat the vaginal lining and inhibit your own natural secretions. Vegetable oils do not appear to cause this problem, and applying vitamin E capsules directly to the vaginal area every night for six weeks, then as and when you need it, may also prove beneficial.

What is it?

The controversial prostate-specific antigen (PSA) test detects raised levels of PSA, an enzyme produced by the prostate and thought to be an indicator of prostate cancer. When the gland enlarges, greater amounts of PSA are produced in the blood. The test is a simple blood test, taking a sample from a vein.

Is it accurate?

As we’ve written before, it’s not clear that the test saves lives. At this time, there are no published randomized trials confirming that early detection improves the long-term prospects for patients with the disease (BMJ, 2004; 328: 301-2):

• It produces a high number of false positives – indicating cancer where none is present – and a high number of false negatives – failing to detect cancer when it’s present (Urologe A, 2000; 39: 22-6). False positives occur mainly in the over-50s, who are more likely to be undergoing regular screening. In this age group, 15 out of every 100 men will have elevated PSA levels, of which 12 will be false positives and only three a true indication of cancer.
• Doctors can’t agree as to what blood level of PSA is significant. The usual cut-off point is 4 ng/mL, but less than that doesn’t automatically mean no cancer. As much as 25 per cent of men with prostate cancer have PSA levels below this.
• The test cannot specify the type of cancer present. Prostate cancer has many forms, with variable growth rates and degrees of fatality; the test doesn’t distinguish between a fast- or slow-growing cancer, or between a harmless and dangerous type. Also, as research has yet to define what constitutes a clinically important prostate cancer, doctors have no clear idea of what the specific target of screening should be.
• The test cannot distinguish a good prognosis. Current test parameters can identify a few men with prostate cancer who have good prospects for long-term survival and a few with poor prospects, but not the vast majority of men with prognoses in between (Ann Intern Med, 2002; 137: 917-29).
• A positive test is usually confirmed by biopsy, another not particularly accurate procedure. Biopsies detect only 40 per cent of those who will go on to develop cancer (Br J Urol Int, 2000; 85: 1078-84).
• Elevated PSA levels can be caused by a number of other factors, including:
  • non-fatal forms of prostate cancer
  • common prostatitis (inflammation of the prostate)
  • benign prostatic hyperplasia, a natural enlargement of the prostate that often occurs with aging
  • medicines for the prostate and the drug finasteride, used to treat male-pattern baldness
  • ejaculation, which can elevate PSA levels for up to 48 hours afterwards
  • any physical activity, especially cycling, which can physically stimulate the prostate to produce more PSA.

Is it safe?

Although the procedure itself isn’t hazardous, a wrong diagnosis can set in motion the entire modern cancer regime, which can be harmful, if not fatal (BMJ, 2004; 328: 301-2). As many as one in six men will be diagnosed with the disease, compared with about one in 29 who will die from it (Ann Intern Med, 2002; 137: 917-29). Prostatic surgery can result in incontinence and loss of sexual function, and hormone treatment can lead to loss of libido and the development of breasts.

Safer uses of the PSA test

• Make sure your PSA test is carried out before a digital rectal examination as physical manipulation of the prostate can stimulate the gland to produce more PSA.
• Find out your percentage of free PSA. PSA circulates in the blood as free PSA and bound to a protein. Men with prostate cancer tend to have less free PSA than men without prostate cancer (Ann Intern Med, 2002; 137: 917-29).
• Use the PSA test only as part of a more comprehensive test for prostate cancer, and consider grossly elevated levels of PSA as only a red flag for further investigations.

Magnesium. A deficiency of this mineral is linked to MVP. Magnesium is necessary for maintaining normal muscle and nerve function, as well as keeping bones strong and heart rhythm steady. One study found that, of 141 patients with heavily symptomatic MVP, 60 per cent showed lower-than-normal levels of blood magnesium. But after five weeks of supplementing their diets with magnesium, the patients experienced significant reductions in symptoms, including physical weakness, chest pain, dyspnoea (breathlessness), palpitations and anxiety (Am J Cardiol, 1997; 79: 768-72).

Magnesium is found in green vegetables such as spinach, and in nuts and seeds. Avoid refined foods such as white bread. Wheat germ and bran are rich in magnesium, but are removed during the processing of white flour. The recommended dosage of magnesium is 200-600 mg/day.

Coenzyme Q10 (ubiquinone). CoQ10 is fundamental to the body’s energy production and for the synthesis of nucleic acids and proteins. Among its various roles, it also enhances heart function. One study treated 424 patients who had various forms of cardiovascular disease, including MVP, by adding CoQ10 to their treatment regimes. Results showed that over 87 per cent of patients showed significant improvement in their everyday heart function and performance. Also, a considerable number were able to reduce the number of different medications they were having to take (Mol Aspects Med, 1994; 15 Suppl: s165-75).

The richest natural sources of CoQ10 are sardines and mackerel, pork, spinach, soya oil, peanuts, sesame seeds and walnuts. To aid its uptake, make sure you have plenty of B vitamins and iron. Avoid stimulants such as caffeine and nicotine, as well as sugar, as they destroy CoQ10. The recommended dosage of CoQ10 is 10-90 mg/day.

L-carnitine. A rich source of amino acid, it plays an important role in strengthening the heart. Italian researchers investigating the effect of L-carnitine in type 2 diabetic patients with essential hypertension found that 2 g twice daily for 45 weeks significantly reduced heart symptoms such as an irregular heartbeat as well as loss of strength (Minerva Med, 1989; 80: 227-31).

Good dietary sources of L-carnitine are dairy, red meat and avocado pears. The recommended dosage is 500 mg/day.

Vitamin E. There are mixed views as to whether this vitamin really can have benefit for potential heart-disease patients. Several observational studies support vitamin E’s role in lowering the risk of cardiovascular disease (Ann NY Acad Sci, 2004; 1031: 280-91). However, the Heart Outcomes Prevention Evaluation (HOPE) study, comparing the ACE-inhibitor ramipril with vitamin E, found that the vitamin did not protect patients against heart problems and chest pain (Cleve Clin J Med, 2000; 67: 287-93). Nevertheless, other studies are ongoing to determine whether a longer period of treatment with vitamin E supplements may be required for any benefit to become evident. The recommended dosage of vitamin E is 200-800 IU/day.

A: Urethral syndrome is a broad term that covers a range of diseases of the urinary tract and bladder. It’s even been called the ‘female prostate’. The condition is very common, and it’s been reckoned that 20 per cent of the female adult population will see their GP at some time with the problem.

Not surprisingly, the syndrome can be triggered by a variety of causes. Often, it is caused by infection sometimes sexually transmitted but this is by no means the whole story: trauma, allergies, age and the onset of the menopause, stress and even muscular abnormalities have all been suspected.

There’s even a small pocket of resistance that regards urethral syndrome as a myth, no doubt the creation of hysterical women seeking attention whereas a similar condition in men is usually referred to as “painful”!

One study found that 80 per cent of all cases are caused by Escherichia coli infection, while fertile women may also be infected by Staphylococcus saprophyticus (Tidsskr No Laegeforen, 1991; 111: 215-8). The most common infection in a study of 237 patients was with Ureaplasma urealyticum, found in 38 per cent of the group. Sexual infections such as herpes and gonorrhoea were also found in a small percentage (Int J Gynaecol Obstet, 1988; 27: 177-80). The bacteria Chlamydia trachomatis is also frequently linked to the condition (Salud Publica Mex, 1992; 34: 301-7).

The standard treatment is a course of antibiotics. In a study of 77 patients, 75 per cent reported improvement with wide spectrum antibiotics, including macrolides and mepartricin (an antifungal and antiprotozoal) (Eur Urol, 1994; 26: 115-9). A three month course of nifedipine, a calcium inhibitor, was also effective (Urol Clin North Am, 1994; 21: 107-11).

Surgery, and in particular urethral dilation, came to the fore 20 years ago, and is based on the theory that the syndrome is caused by anatomical problems (Minn Med, 1990; 73: 33-4). It is an approach that has fallen out of favour among urologists who left medical school less than 10 years ago. A questionnaire among 194 urologists in the US found that 60 per cent of those trained in recent years would never consider dilation as an option. Interestingly, 21 per cent trained more than 10 years ago thought dilation was “very or extremely successful” in treating the syndrome whereas none of the group trained more recently shared that view (Urology, 1999; 54: 37-43).

Of all the alternative treatments, acupuncture helped to improve the condition in 128 patients better than standard Western treatment given to 52 other sufferers (J Trad Chin Med, 1998; 18: 122-7).

There’s also a wide range of alternative remedies that can help relieve symptoms of urinary tract infections, including cranberry juice, vitamin C (although this can aggravate the condition in chronic cases), tea tree oil, and herbs such as buchu, burdock, coriander, cornsilk, Echinacea and juniper berries (Alternative Medicine, Tiburon, California: Future Medicine Publishing, 1999).

CPT: Portal to payment, owned by the AMA

Integrative nursing leader Mary Jo Kreitzer, RN, PhD sent
a message last week wondering if I knew the exact number of millions of dollars
the American Medical Association (AMA) makes each year via ownership of the Current
Procedural Technology (CPT) codes through which third party payment is
managed in US health care.

Kreitzer, who founded and directs the Center for Spirituality
and Healing at the University of Minnesota, was provoked to ask by the latest
evidence of AMA opposition to independent practice by nurses. On October 5,
2010, the Institute of Medicine (IOM) published a long-awaited report entitled
The Future of Nursing: Leading Change, Advancing Health. The multidisciplinary
IOM team presented the vision of a future in which nurses, without supervision,
will provide a significant portion of the nation’s primary care. Nursing
supporters welcomed the study as opening a “golden age of nursing.”

AMA: Developed the CPT in the first years of Medicare in the mid-1960s

The AMA met the IOM findings with a Jaggeresque chorus of
“under my thumb.” The AMA’s concern was couched as interest in the public safety.

Clearly, the AMA was not about to have its paradigm
shifted by recommendations from the agency that is called the “brains of US
medicine.” Never mind that the IOM report concluded that there was a lack of
evidence to support the charge of safety concerns in independent practice by
nurses.

Instead, the AMA-as-guild responded with the same lower chakra
behavior enshrined in the organization’s infamous 2006-present Scope of
Practice Partnership (SOPP) campaign.  Via
the SOPP, the AMA supports and organizes opposition to scope expansions of all
other professions, including chiropractic doctors, midwives, psychologists,
naturopathic physicians, optometrists, acupuncture and Oriental medicine
practitioners as well as advance practice nurses. The AMA also opposes the anti-discrimination portion (Section 2706) of the Obama reform law.

Kreitzer: AMA opposition to nurses led her to call the question

This gets us back to Kreitzer’s question, and the
question within it: Why are all practitioners
routinely paying the AMA if the AMA can turn around and use these funds to
attack these profession and any ideas the AMA doesn’t support?

Establishing the exact size of the AMA bonanza from CPT royalties
is challenging. Web searching finds a July of 2001 letter from then US Senate
Minority Leader Trent Lott (R-Miss) to then US Secretary of Health and Human
Services Tommy Thompson.  Amidst a series
of probing questions about the AMA and the CPT, Lott cites the Wall Street Journal in placing at
$71-million the AMA’s “financial windfall in the form of CPT-related book sales
and royalties.” A Republican activist blogging in July 2009 on her view that
AMA’s ownership of the CPT is part of why “the AMA sold out doctors and
patients for Obamacare” puts the figure at $118-million. She offers no sourcing
of this amount and she did not respond to a query.

I contacted the AMA.
A communications staffer shared that “the 2009 AMA
Annual Report does not breakout CPT revenue from the total revenue
generated by the complete line of AMA books and products.” According to the report, the CPT “and more than
100 other books and products” generated $70.9 million in revenue in 2009.

AMA doesn’t make it easy to see how many tens of millions the CPT generates

This
seems low, if the Wall Street Journal and Senator Lott were correct in using roughly the same figure 9 years ago.

Notably,
the $71-million does not include $47.5-million in 2009 revenues from “Database
Products.” Might this separate category include the AMA’s downloadable CPT products? I have
not heard back from the AMA. [I heard from the AMA’s media relations the day after this was published. The response was as follows:

“No other categories
include CPT related revenues. All CPT revenues
are included with revenues generated by the complete line of AMA
books and products … The AMA Annual Report is
the only source of publicly available information on the AMA’s finances.”

These direct financial benefits do not include indirect values of the
AMA’s CPT ownership. For instance, AMA members are offered steep discounts on CPT product purchases,
effectively lowering the price of membership.

More
importantly, CPT ownership means that the AMA controls the ability of any other
professions, whether nurses or chiropractic physicians or naturopathic doctors or optometrists,
to create any new codes to better reflect their practices for the purposes of
payment. And via CPT ownership, the AMA is
married to the Centers for Medicare and Medicaid Services on scores of payment-related
issues.  

Another of the AMA’s CPT products

Never mind the clout for a moment. This
is a good deal of money to the AMA. The $71-million figure is 26% of the AMA’s
total revenues of $269-million in 2009. These revenues amount to 157% of the
$45-million portion of its income from membership dues paid by the 17% of
medical doctors who choose to join. (The other significant income categories were
$56-million for advertising and $35-million for insurance products.) For
additional perspective, direct federal lobbying costs by the AMA in 2009 amounted
to just over $20-million. This figure doesn’t include any Scope of Practice
partnership activities in individual states or the myriad of “educational”
activities that the AMA engages to influence policy but that are reflected
directly as direct lobbying costs.

To recap: 

• All
  guilds must use the CPT if they want to participate in 3^rd party
  payment.

• To do so, they must pay one guild, the AMA.
  
• This guild is pitted against
  their efforts to expand their practice scopes. 
  
• In
  addition, this guild is apparently opposed to multidisciplinary recommendations from the brains
  of US medicine about the future of healthcare in the United States.
  
• As is clear in
  the IOM report, many medical doctors are not aligned with the AMA position. In
  fact, the AMA that received these $71-million+ each year presently counts only
  15%-20% of MDs as dues-paying members.

I sent an email to Kreitzer once I began to get a sense
of the dimensions of the CPT’s value to the AMA, asking for a comment on why she
felt this important. Kreitzer wrote:

“It is hard to
imagine real health care reform without having reform of the system that has
been used to drive payment and reimbursement. The system we have has been
controlled by the medical profession. It has incentivized medical professionals
to offer tests, procedures and services that match codes and maximize
reimbursement.

“Historically, it has been very difficult for advanced practice
nurses and integrative care practitioners to secure access to the codes which
then limits the public access to a broader array of providers and services. I
think that there needs to be transparency on how much income the AMA generates
annually from [the CPT] that essentially drives medical practice and constrains
the practice of other professionals. And clearly, it is time for payment
reform. Without payment reform, there will be no true health reform.”

Transparency is good, but doesn’t go far enough. The necessary transformation of US healthcare
is toward diversity, multidisciplinary practice, collaboration, team-care, and
respect for the skills of all parties. The movement is away from the still current patriarchal,
top-down, MD-centric, father-knows-best world of Dr. Kildare. The movement is definitely away from any belief set allowing practitioners of all stripes to tithe to a small minority of rear-guard
AMA fighters who have taken it upon themselves to stand in
the way of reform. 

There is no more powerful emblem of the guild-uber-alles healthcare world that causes such problems in optimal care than the AMA’s CPT
ownership. Part of the “payment reform” for which Kreitzer calls must be wresting this control from a single guild. The present system, akin to
taxation without representation, may have made sense before organized medicine
was challenged by the rise of nursing, of other (increasingly non-) allied health
care professions and integrative practice disciplines.

It’s time for a CPT party revolt to claim these tools as rightfully part of a jointly-held commons.

There’s been a quiet revolution taking place in the food-manufacturing industry since the 1980s, and it’s one that could be damaging our health and making us overweight. Indeed, the new evidence suggests that it may even be responsible for the learning and behavioural problems so often seen in our children nowadays.

Over the past 30 years, food manufacturers have slowly been replacing sucrose as a food and drink sweetener with high-fructose corn syrup (HFCS)-or ‘glucose corn syrup’ as it’s known in the UK.

In 1970, more than 83 per cent of the sweetener consumed in the US was sucrose. However, according to OU (Orthodox Union) Kosher – a non-profit communal organization based in New York City-by 1997, sucrose-containing food and drink had dropped to just 43 per cent, with 57 per cent using HFCS instead.

OU Kosher has a logo – a U in a circle – that, when seen on a label or packaging, means that the food has been officially certified as kosher (see http://www.oukosher.org for more information) and, in order to obtain
this certification, the food company must submit a complete list of the food’s ingredients.

In the UK, the Institute of Food Research, based in Norwich, has described HFCS as “a brilliant technological invention”, as it has many advantages over traditional sweeteners.

In addition to its ability to lengthen the shelf life of products, it blends more easily into liquids and keeps its sweetness better than sugar. For this reason, it was quickly adopted by Coca-Cola, Pepsi and other soft-drink manufacturers. Also, it helps to stop food ‘freezerburn’ as it prevents icy crystallization and so is used in frozen products such as ice cream. What’s more, it helps to turn baked goods brown, and so is used in cakes, pastries, bread rolls, crackers and breakfast cereals. Most important of all, it’s far cheaper to produce than other sweeteners.

Nowadays, it is found in virtually every processed food and drink – from Coca-Cola, Pepsi, Kellogg’s Cornflakes and its other breakfast cereals to some Ben & Jerry’s ice creams, Campbell’s Vegetable Soup, processed breads and cakes, Ribena, Ocean Spray Cranberry Juice – and many other products as well.

Best of all, claim its advocates, it’s both natural and safe, a view that is supported by America’s foods regulator, the Food and Drug Administration (FDA). Indeed, most scientists and commentators apparently agree. Nevertheless, there are a few who believe that HFCS-enriched foods and drinks are a direct cause of obesity and diabetes.

However, while the experts continue to debate whether or not HFCS is contributing to the growing obesity and diabetes pandemic, a recent report has now discovered a much more serious health concern: the sweetener evidently contains mercury, and may be a richer source
of the toxic heavy metal than even fish.

Corn Syrup and Mercury

While the FDA continues to maintain that HFCS is a safe food additive, other investigators have been uncovering evidence that clearly suggests otherwise. One such investigator was Renee Dufault who, in 2005, found mercury levels in nine of the 20 HFCS samples that she had collected from processing plants. However, the FDA did nothing in response to her findings, leaving her no choice but to go public with the information after she retired last year.

Dufault had discovered levels of mercury ranging from 0.005 to 0.570 micrograms (mcg)/g of HFCS and, as the average daily consumption of the sweetener is around 50 g in the US, consumers are very likely – and unwittingly – ingesting every day up to 28.5 mcg of mercury, the most toxic metal known to man.

As the standard 20-oz bottle of Coca-Cola contains around 17 teaspoons’ worth of HFCS, it’s easy to see why processed snack foods and soft drinks are easily a far higher source of mercury than are fish (Environmental Health, 2009; 8: 2; doi: 10. 1186/1476-069X-8-2).

But how did the mercury get into the HFCS amples in the first place? Although its advocates describe HFCS as ‘natural’ and even ‘organic’, it’s nothing of the sort. While other sweeteners are based on cane and beet sugar, HFCS is a derivative of corn starch-and it comes about only as a result of various industrial processes.

In 1957, scientists discovered an enzyme that could convert the glucose in corn syrup into fructose, a process that was finally perfected only in the 1970s, thereby paving the way towards mass production of HFCS.

The process involves several steps and three different enzymes, and the result is a syrup with a 90-percent fructose content. This is then blended down with untreated, glucose-only syrup into a mix that is either 42-per-cent or 55-per-centfructose.

Around 50 processing plants around the world, including eight in the US and three in the UK, are currently producing HFCS. And some of these plants-more correctly known as ‘industrial chlorine’ or ‘chlor-alkali’ plants – still use caustic soda (sodium hydroxide) in the manufacture of HFCS, although it’s an outmoded form of manufacturing and some plants have replaced it with safer technology. Other food ingredients, such as citric acid, are also manufactured at these plants.

The caustic soda is referred to as ‘mercury-grade’ or ‘rayon-grade’, which indicates that these plants are reliant on mercury for part of the process. Astonishingly, the plants regularly report that some of the mercury mysteriously disappears. In the year 2000, for example, the four plants in the US that still use caustic soda each reported an unaccountable loss amounting to around seven tons of mercury.

What’s more, the three UK plants report a similar story, although the environmental lobby group Oceana believes that the mercury loss isn’t so mysterious, and that it’s pumped out into the air and into the general water supply.

In fact, according to the group’s report Poison Plants, published in January 2005, these three plants are responsible for a third of all mercury emissions in the air and nearly half of all emissions in the water supply of the UK.

Nevertheless, the release of mercury into the environment accounts for only a mere fraction of the total mercury ‘lost’. In 2003, nine of the mercury-using plants around the world reported that eight tons of the stuff had been emitted into the air and water supply. Nevertheless, they still could not explain the disappearance of a further 30 tons to the US Environmental Protection Agency for its 2003 report [68 FR (Federal Register) 70904].

In light of these facts, it’s not an enormous leap of imagination or judgement to suspect – given such cavalier safety procedures – that some of the so-called missing mercury may well be getting into the HFCS itself, as Dufault and her colleagues discovered.

Snacking on Mercury

Alerted by Dufault and her colleagues’ findings, Dr. David Wallinga and other researchers at the Institute for Agriculture and Trade Policy (IATP), an independent lobby group based in Minneapolis, MN, went out and bought a range of commonly consumed soft drinks and snack foods sweetened with HFCS, and tested them for mercury.

Of the 55 products they purchased from the local supermarket, the researchers found that one-third contained mercury, including products made by Quaker, Kraft and Nutri-Grain-all international and well-known brands.

The levels of mercury varied enormously, with the highest level being twice the amount of the lowest. The highest amounts were found in barbecue sauces, whereas the colas and soft drinks contained no mercury.

Nevertheless, Wallinga and the other IATP researchers strongly emphasize in their report – Not So Sweet: Missing Mercury and High Fructose Corn Syrup, published in January 2009 – that their findings are only a snapshot based on just a one-off purchase.

More important, they believe that the food and drink manufacturers are probably unaware that their products contain mercury, and they may not even be aware that mercury grade caustic soda is being used in the processing of the sweetener. And judging by the website of the UK’s HFCS industry group, the IATP may have a point.

Indeed, on its website (www.highfructosecornsyrup.co.uk), the group reiterates that the FDA regards HFCS as a “natural product as the only two elements present in HFCS are fructose and glucose. Both fructose and glucose are naturally occurring sugars, and they also happen to be the sugars which form the disaccharide sucrose, which is commonly known as sugar”. While this is true as far as it goes, the HFCS advocacy site fails to mention that the sweetener is derived from corn syrup, a glucose heavy product that would never
contain fructose in its original form.

In other words, the “natural” claim is being used out of context: fructose is indeed natural, but not in association with corn syrup. In addition, there’s no mention of the industrial processes involved in getting fructose into the product.

The Industry Response

American corn producers have been one of the chief beneficiaries of the explosion in HFCS usage, so it’s not very surprising that its industry group, the Corn Refiners Association (CRA), was quick to refute
Dufault’s findings. It did not, however, respond to the IATP study and its discovery of mercury in a substantial number of snacks sweetened by HFCS.

CRA’s president, Audrae Erickson, says the Dufault study is based on “outdated information of dubious significance”. She claims that the industry has used mercury-free processing plants for several years –
and yet, according to the IATP, four of the eight plants in the US still use mercury-based technology – and there may be many more plants around the world that are still reliant on mercury.

Erickson also reports that the FDA deemed HFCS safe in 1983 and again in 1996, although it was not made aware of Dufault’s findings until 2005-since which time it has not issued any new statements on the safety of HFCS.

Erickson concludes by repeating the claim that HFCS is “natural” as it contains no artificial or synthetic ingredients or additives. However, it appears to be somewhat of a stretch to claim that any product is natural when it has passed through three industrial processes and used enzymes to create its final form. As Michael Jacobson, director of the Center for Science in the Public Interest, a US nutrition advocacy group, has said: “You’re causing a change in the molecular structure and that shouldn’t be considered natural.” Instead, he believes that HFCS should be reclassified as an artificial sweetener.

The Mercury Load

While we the general public are generally aware of the amount of mercury we are exposed to from the fish we eat and the amalgam in our dental fillings, no one so far has taken into account the additional mercury load we may be unwittingly ingesting from our snacking and drinking habits. If Dufault and her co-workers are correct in their analyses, the average person is swallowing an additional 28.5 mcg/day of mercury – and this figure may be even higher among teenagers, as they tend to eat more snack foods, and drink more colas and sodas.

Nevertheless, some critics accuse Dufault and the IATP of being alarmist. Toxicologist Carl Winter, of the FoodSafe Program at the University of California at Davis, says that the most toxic form of mercury is methylmercury, the type found in the fish we eat, as this form is more easily absorbed into the body. It’s possible, he says, that Dufault and Wallinga have been measuring elemental mercury, which is not so
dangerous.

Even so, there’s no such thing as ‘safe mercury’ in any form, and high doses can cause damage to the heart, kidneys, lungs and immune system. Furthermore, this unsuspected additional mercury load from snacks and soft drinks might also be a contributory factor to the alarming rise we’ve seen in recent years of cases of attention-deficit/hyperactive disorder (ADHD), autism and behavioural problems among our youngsters.

As Wallinga says, “For me, the take-home message is really that this [HFCS] is a totally avoidable, unnecessary exposure to mercury.”

Bryan Hubbard

Electromagnetic fields (or EMFs) from electricity lines almost certainly cause leukaemia, Alzheimer’s disease and other degenerative illnesses. Yet, most scientists—and every power supplier and government planning department around the world—continue to deny that power lines are a health hazard.

The International Agency for Cancer Research of the World Health Organization (WHO) has classified extremely low-frequency (ELF) EMFs as a possible carcinogen (cancer-causing agent) in light of the overwhelming evidence that has been uncovered in recent years. Indeed, the Agency’s latest position, reported in 2001, is a complete reversal of its stance of four years ago, when it agreed with most scientists that there is no evidence of a causal link between power lines and severe illnesses. The WHO also recommends that power lines be sited well away from homes “to reduce people’s exposure”.

In the UK, the government-funded advisory group SAGE (Stakeholder Advisory Group on ELF EMFs) reported in 2007 that there is now sufficient evidence of a causal link between power lines and childhood leukemia for power companies to adopt a precautionary approach. In particular, SAGE recommends that, in future, power lines should be placed underground, and that no new homes should be built within 60 metres of existing power lines.

It’s a view shared by the State of California, which commissioned a $7m, 10-year review of power- line safety in 1993. The study, called the ‘California EMF Project’ (2002), concluded that magnetic fields from power lines and other sources are a likely cause of childhood and adult leukemia, adult brain cancers, spontaneous abortions and ALS (amyotrophic lateral sclerosis), the degenerative disease that afflicts astrophysicist Dr Stephen Hawking.

The EMF Project researchers state that “even a slight additional lifetime risk could be of concern to regulators, who already regulate other environmental concerns that convey even lower risks.”

So why do scientists persist in remaining ambivalent over the research-based evidence, and why are governments, regulatory bodies and power suppliers refusing to act when they must certainly be aware that overhead power lines represent a reasonable health risk?

Before we answer these questions, let’s look at some of the studies published since 2000, the watershed year that heralded the beginning of all the research that began to draw compelling links between EMFs and their effects on the human immune system.

Power lines and leukemia

The possibility that power lines cause childhood leukemia has attracted more research than any other health concern associated with EMFs.

One of the strongest associations was established by what is now referred to as the ‘Draper report’, a case-control study that discovered that children under the age of 15 years who lived within 100 metres of power lines were nearly twice as l i kely to develop leukemia compared with children who lived further away (BMJ, 2005; 330: 1290–4).

The team of researchers, led by Gerald Draper and based at the University of Oxford, included a representative from the National Grid Transco plc as scientific advisor. They arrived at their conclusions after examining the profiles of 29,081 children who developed
cancer between 1962 and 1995 in England and Wales.

Although the findings were of considerable public interest, the UK Government’s Department of Health, which had funded the research , suppressed the report for four years. Officials at the Department were first informed of the preliminary results in 2001, yet the report was not
published until June 2005.

What’s more, even when it finally made it into print, Geoff Watts , science editor of the British Medical Journal, declared that the Draper report simply means that only “five cases annually of childhood leukemia may be associated with power lines” compared with the 32 children who are killled annually in house fires or the 200 who die every year on UK roads (B M J, 2005; 330: 1294–5). Nevertheless, it was still an admission that power lines can affect
our health.

Two researchers—Anders Ahlbom f rom the Karolinska Institute in Stockholm and Sander Greenland from the UCLA School of Public Health in Los Angeles, CA—h a v e
conducted a range of studies into EMFs and childhood leukemia since 2000. Indeed, in that year alone, they both published papers – one of which was a pooled analysis of 15 studies— that demonstrated a doubling of leukaemia rates among children exposed to the same levels of ELF fields as are generated by standard power lines (Br J Cancer, 2000; 85: 692–8;
Epidemiology, 2000; 11: 624–34). A year later, Ahlbom followed up with another review of the “voluminous epidemiologic literature on EMF” that confirmed the association of childhood leukaemia and postnatal exposures to EMFs (Environ Health Perspect, 2001; 109 [Suppl 6]: 911–33).

Power lines and Alzheimer’s

Several studies have produced compelling evidence for a causal connection between EMFs and Alzheimer’s disease. The latest study, published in November 2007, comes from Switzerland, where researchers have established that people who are living within 50 metres of a power line for 15 years or more have twice the the risk of developing Alzheimer’s
disease compared with those who are living 600 metres or more from such power lines.

Researchers at the University of Bern made the discovery when they analyzed the health profiles of 4.7 million people in Switzerland who lived close to a power line. They concluded that the distance from a line, and the duration of time spent living near such a line, were both
significant risk factors. The overall risk of Alzheimer’s for anyone living within 50 metres of a power line for any length of time was 1.24 times greater than that of someone who lived further away (Am J Epidemiol, 2008; doi: 10.1093/aje/kwn297).

In fact, the conclusion that the duration of EMF exposure is asignificant marker of Alzheimer’ s
risk has been supported by a study of workers in Spain whose occupations bring them into regular contact with ELF EMFs. A meta-analysis of 14 studies, carried out by researchers at
Valencia University, revealed that people in those occupations had twice the risk of developing Alzheimer’s in later life compared with the general population (Int J Epidemiol, 2008; 37: 329–40).

EMFs and other diseases

As EMFs are believed to interfere with the workings of the immune system, it follows that they would be expected to be responsible for causing a wide range of degenerative, chronic diseases, as suggested by California’s EMF Project findings. In fact, in addition to leukemia, the researchers consider it “likely” that magnetic fields are the cause of spontaneous abortions (miscarriage) and ALS, a view that has been supported by a number of studies.
Three recent studies support the hypothesis that EMFs cause spontaneous abortions. One such study, which reviewed 177 cases of miscarriage in Northern California, found a close correlation with exposure to high levels of EMFs. Women exposed to the highest levels
were more than three times more likely to miscarry than those whose exposure was minimal (Epidemiology, 2002; 13: 21–31).

Scientists at the Kaiser Foundation Research Institute in Oakland, California, arrived at a similar conclusion when they examined the cases of 969 women from the San Francisco Bay area who had experienced miscarriage. Although they could find no correlations among
women exposed to average levels of EMFs, those who were regularly exposed to levels of 16 mG (milliGauss) or more were nearly twice as likely to lose their pregnancy (Epidemiology, 2002; 13: 9–20).

The third study, carried out on laboratory mice, demonstrated that exposure to ELF EMFs during pregnancy would not only affect the term of the pregnancy, but could also interfere with the development of the offspring (Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi, 2006; 24: 468–70).

Further studies also suggest that high EMF levels may cause ALS. The first, which analyzed the Swedish census of 1980 against instances of neurodegenerative disorders such as
Alzheimer’s disease and ALS, found that workers in the electrical or electronics industry had a 40-percent greater chance of developing ALS than those who did not work in electrical/electronic-related occupations (Epidemiology, 2003; 14: 413–9).

The Swedish study findings were supported by a later study that also found a direct correlation between exposures was more than two times greater than for those in other industries, although the risk was higher still – at four times – for Alzheimer’s disease (Epidemiology, 2003; 14: 420–6).

In yet another study, the researchers concluded that “there are relatively strong data indicating that electric utility work may be associated with an increased risk [of ALS]” (Bioelectromagnetics, 2001; suppl 5: S132–43).

Why scientists disagree

Power lines emit both electrical and magnetic fields. The electric field is related to the voltage running through the line—a typical cable handles between 275 kV (kilovolts) and 400 kV -whereas the magnetic field is dependent on the current being carried through the cable, and
this can vary depending on the usage. This means that any scientist researching the impact of an EMF is faced with the immediate problem of how to measure something that can fluctuate wildly over any 24-hour period. This is why only studies that have examined EMF effects over years are able to discern any causal relationship with health problems, whereas a study that is carried out for only a few days or weeks at a time is only able to determine insignificant
effects—if any at all.

Scientists who deny any association also argue that no one truly understands how EMFs can cause cancer or damage the immune system. However, as Alasdair Philips of Powerwatch, an independent consumers’ information service, says: “We still do not know the actual
mechanisms by which cigarette smoking, asbestos fibre or DDT cause cancers, but we have accepted the epidemiological evidence and have introduced laws to limit or reduce
human exposure.”

The distance from power lines is another issue, and sceptics have argued that people living even relatively short distances from them should not suffer any ill effects. In effect, they appear to be suggesting that illnesses being reported may just be psychosomatic—all in the
head.

Professor Denis Henshaw, at Bristol University, has spent years studying this issue, and has come up with an hypothesis of ‘corona ions’. He posits that the ions emitted by
high-voltage power lines are ending up as tiny charged particles of air pollution that can penetrate deeply into our lungs and bloodstream. These so-called corona ions are
carried on the wind and quickly become attached to microscopic particles of air pollution, thereby electrically charging them.

Professor Henshaw believes that these pollutants can be carried several hundred metres away from power lines, which would explain why children living at greater distances –
and downwind—from a line can stilldevelop leukaemia.

One task of the BioInitiative Report, prepared by 14 independent internationally based scientists in 2007, was to try to understand why there is still so much disagreement
among experts, despite the fact that enough evidence has already been published to justify improvements in safety standards within the power industry.

Among the 10 reasons listed by the Report, the authors concluded that:

• different scientists use different measurements to determine the existence of any proof;
  
• some scientists continue to insist that every study should achieve the same results;
  
• some scientists are only looking at short-term and acute effects, which do not always tell the whole story; and
  
• vested interests appear to have a substantial influence on the whole issue under debate.
  

Industry pressures

This is an exceedingly high-stakes game, one that goes way beyond deciding whether power lines should be buried under the ground or not. If governments and power industries
accept the growing epidemiological evidence that EMFs cause cancer—not to mention any other chronic and degenerative diseases—then there will need to be a massive change in
the way we live our lives.

EMFs are emitted from the mains electricity and all the wiring in our homes—powering everything from microwave ovens to Wi-Finetworks—but also, and more significantly, from
mobile phones and mobile-phone masts.

The upshot of all this is that, while it is a matter of degrees and being reasonable, any admission from our health guardians that EMFs are causing cancer would have major
effects on the world’s economy—not to mention our present taken—for granted
comfy lifestyles. It is also known that the power industry, like the drug industry, recruits and richly rewards ‘friendly’ scientists who are always on hand to deride any research
that links EMFs to cancer and other diseases. Indeed, the power industry openly—but sometimes covertly—funds research that invariably discovers no association between
EMFs and illness.

This is part and parcel of the damage limitation that began in the 1960s, when field pioneers such as Drs Ross Adey, Milton Zaret and Robert Becker started investigating the effects of EMFs on humans. Dr Zaret was among the first to discover that EMF radiation, such as
emitted by microwaves, is biologically harmful and can cause conditions such as cataracts. Yet, in the course of his work, his research funds were stopped. Dr Becker worked for the
US Navy, and his brief was to assess the health impact of a submarine ELF communications system. His study concluded that the health of significant segments of the American
population was at risk from 60-Hz power lines. But when the State of New York was planning the construction of 10 high-power lines, the Navy denied that Becker’s work existed, so
the high-power lines were erected. Becker said afterwards: “The way science is currently funded andevaluated, we are learning more and more about less and less, and science
is becoming our enemy instead of our friend.”

Dr Adey, who died in 2004, worked on secret CIA projects in the 1970s that looked into the impact of EMFs on people’s mental health. Since then, other researchers have found that these energy fields can cause depression: indeed, several noted that suicide levels were far higher among people who lived near power lines.

In 1992, Adey reported that there was “very little doubt” that EMFs affect the immune system, interfere with fetal development and cause birth abnormalities, damage healthy cell growth, encourage tumour formation, and affect the central nervous system and the brain. In addition, as he said on BBC Radio Scotland on January 10, 1992, “This work is being carried out in
many laboratories worldwide so that the old fiction that this research describes uncorroborated experiments is no longer true.”

In the 16 years since that programme was aired, the evidence has become even stronger, but it will still be a long time before governments and the so-called guardians of our public health admit it. As Dr John Bonnell, chief medical officer for the UK’s now-defunct Central Electricity Generating Board, said in 1985, on a Central TV programme entitled The Good, the Bad and the Indefensible: “If we accepted the dangers, it would mean an enormous turnabout for industry and for the country as a whole. There are no contingency plans to cope with such
a turnabout.”

Not only are there no contingency plans in place, but we have also seen the explosion of the mobile-phone industry in the intervening years, making any admission concerning the harmful effects of EMFs physically as well as fiscally catastrophic.

Bryan Hubbard

The first cases of Lyme disease (LD) occurred in the US, but it’s now acknowledged to be a worldwide problem. Britain had its first official death due to LD in December 2005: “liver disease due to Lyme sepsis”, according to the autopsy. In May of this year, a 38-year-old British professor committed suicide after developing dementia brought about by LD. It’s particularly prevalent at this time of the year-late spring and early summer.

The number of diagnosed cases of Lyme disease are now rising – and not just because doctors are finally beginning to recognize it, but also possibly as a result of global warming. And, as with many new-disease discoveries, a whole raft of previously mysterious conditions are now being laid at the door of LD, including chronic fatigue (CFS/ME), multiple sclerosis (MS) and even autism. Could we be witnessing the start of a new epidemic? “Many of the diseases that are considered incurable by conventional medicine may have some kind of Lyme component,” says American alternative practitioner Dr Lee Cowden.

What is Lyme disease? In essence, it’s a kind of malaria, although it emerges not from the swampy jungle, but from temperate forests. Like malaria, the disease is transmitted by being bitten by a blood-feeding creature-in the case of LD, not by an insect, but a tick, an arachnid, that lives on animals such as cattle, birds and even mice, but primarily deer.

Where it all began
Lyme disease first appeared more than 30 years ago as a mysterious disease outbreak in an American town called Lyme, in Connecticut. In the spring of 1975, there was a cluster of cases of what appeared to be juvenile arthritis. Children as young as 10 began to develop severe joint pain. Doctors from nearby Yale University were called in to investigate, and were puzzled by the appearance of odd rashes on the children’s skin. Months of detective work finally led the doctors to connect the symptoms to a disease that had first been described in Europe almost a century before as ‘sheep-tick fever’.

After years of further detective work, researchers traced the illness to a rogue spirochaetes bacterium in the patients’ blood known as Borrelia burgdorferi-hence, the alternative name of ‘Lyme borreliosis’. But where had it come from? Already alerted to the fact that it might be due to a tick bite, the scientists began a hunt among the local animal population. The Borrelia microorganism was finally tracked down to a tick of the genus Ixodes that lives on deer. This tiny arachnid-related to mites, spiders and scorpions, having eight legs-has a correspondingly tiny mouth, so its bite is rarely felt, which may be one reason why it was able to elude detection for so long. Ixodes is also cleverly able to inject its prey with a local anaesthetic, further disguising its attack. In fact, most victims of Lyme disease have no idea they were ever on the tick’s hit list.

In fact, it’s likely that Ixodes has to remain undetected because it’s believed to be an inefficient feeder. It needs to be plugged in to its prey for hours to obtain sufficient nourish-ment. One indication of this is the probability that B. burgdorferi is not transmitted until the tick has been attached for at least 12 hours.

Initially, medicine treated the disease just like any other bacterial infection-with antibiotics. These appeared to work, and doctors patted themselves on the back for having put paid so easily to this novel disease. But the story hasn’t turned out to be that simple.

Although this medical field is still relatively small, there is already a schism appearing among LD clinicians; indeed, some would call it a war. One army of experts believe that Lyme disease can be easily cured by a short course of antibiotics, whereas the opposing side says no, LD is a complex, potentially long-term illness.

The problems begin with the diagnosis. If LD is spotted early on, then antibiotics can prove helpful. But, in practice, LD turns out to be very difficult to diagnose, and the later stages of the disease are much harder to treat with the usual drugs.

What’s more, these antibiotics can sometimes make things even worse. Any Borrelia bacteria that are not totally killed off by the drugs don’t just develop resistance-which is bad enough-but also become what is referred to as ‘cell-wall deficient’. This makes them very elusive as, without walls, they can hide inside of healthy cells, thereby avoiding direct attack by the drugs (Infection, 1996; 24: 218-26).

Lyme patients also find that the types of antibiotics used to treat them may actually exacerbate their symptoms. This is thought to be the result of changes due to the drugs in the genetic sequencing of Borrelia, causing them to release toxins into the body. These toxins often get into the brain and nervous system, precipitating what is called the Jarisch-Herxheimer reaction (named after Karl Herx-heimer, the German dermatologist who first observed it). J-H reactions can be life-threatening, and are seen
in one in seven Lyme borreliosis patients treated.

The leaky brain
In fact, it has also been suggested that LD in itself-whether treated by antibiotics or not-may be neurotoxic. The idea is that Lyme disease creates ammonia in the brain, causing a ‘leaky-brain syndrome’. Among the first to propose the idea was LD specialist Dr David Jernigan. As ammonia can alter permeability of the blood-brain barrier, he says, it would allow large molecules to reach the brain, causing ‘cerebral allergies’. Jernigan believes that this may be a major cause of a variety of LD symptoms (Townsend Lett Docs, 2007; April: 141-8; online only).

Confirmation of this hypothesis has come from animal studies. Using radioactive tracers, researchers have shown that laboratory animals, when infected by Borrelia, lose the pro-tection of the blood-brain barrier
after just two weeks (Schutzer SE, ed. Lyme Disease: Molecular and Immunologic Approaches, Series 6. Current Communications in Molecular and Cell Biology. Plainview, NY: Cold Spring Harbor Press, 1992)

How does Borrelia do this? It’s thought that the bacteria burrow their way between the cells of the brain’s outermost membrane, causing a localized inflammation that, in turn, releases proteins to fight against the bacterial invasion; this then results in holes in the cerebral membrane. It’s much the same mechanism as seen in the leaky-gut syndrome but, in this case, it’s potentially more serious as it involves the brain.

In addition, there is now laboratory evidence that Borrelia can “attach to or invade human cortical neuronal cells”, say researchers at the National Center for Infectious Diseases in Colorado, part of the US Centers for Disease Control and Prevention (CDC). This makes the bacteria difficult to kill by the immune system (Microbes Infect, 2006; 8: 2832-40). It also helps to explain why Lyme disease can be both relapsing and resistant to treatment.

Incidentally, the spirochaetes bacterium that causes syphilis has a similar mode of action and can also lodge in the brain, potentially remaining active for years.

Brain abnormalities
The leaky-brain theory also accounts for some of the highly specific neurological abnormalities found in Lyme patients-including Bell’s palsy, lymphocytic meningitis, meningo-encephalitis and cranial neuritis-not to mention the less specific CFS/ME and ‘brain fog’.

“The neurological and psychiatric manifestations of Borrelia are so numerous that it is called the ‘new great imitator’,” says Dr Frederic Blanc, of the University of Strasbourg, France. “Every part of the nervous system can be involved: from central to peripheral nervous system, and even muscles” (Med Mal Infect, 2007; Mar 8; Epub ahead of print).

In fact, as long as 10 years ago, LD was firmly characterized as a ‘neuropsychiatric illness’. Reviewing the whole history of the disease, a team of psychiatrists at New York’s Colum-bia University found Lyme disease to be responsible for “a broad range of psychiatric reactions”, including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa and obsessive-compulsive disorder (Am J Psychiatry, 1994; 151: 1571-83). Since then, tests have discovered reduced blood flow in the brains of chronic LD sufferers, explaining the impaired mental functioning that afflicts so many victims of the disease (Neuro-psychiatry Clin Neurosci, 2003; 15: 326-32).

The autism connection
The most dramatic mental condition thought to be caused by Lyme disease is autism. A rare condition 50 years ago, autism now affects one in every 150 American children, according to the latest figures from the CDC. But why should Lyme disease be implicated? One of the first clues was that the psychological symptoms of LD are similar to those of autism.

Six years ago, the above-mentioned Columbia University psychiatrists found that children with Lyme disease have “significantly more cognitive and psychiatric disturbances . . . resulting in psychosocial and academic impairments” (J Neuropsychiatry Clin Neurosci, 2001; 13: 500-7).

There are other clues, too. As already mentioned, syphilis, which is caused by a similar spirochaetes as in LD, in the womb is known to cause autism. Furthermore, autistic children are known to have many metabolic dysfunctions which are shared by victims of LD, in particular, chronically low counts of CD57 natural-killer (NK) cells.

Of course, scores of theories have been proposed for the cause of autism, among which vaccine damage is perhaps the best known. But LD may be involved there, too. “It is possible that the two are conjoined in damage, and the long-term effects of Borrelia could hamper the body’s ability to mount a significant, timely response to vaccines,” says Dr Geoffrey Radoff, of the Alternative Medical Care Center of Arizona. “This could explain the higher incidences of adverse reactions to vaccinations in children with autism (Townsend Lett Docs, 2007; April: 78-81; online only).

However, some children appear to be born with autism, so how could Lyme disease be involved there? Although the research has yet to be done in humans, studies of farm animals have shown that Borrelia can pass through the placental barrier into the womb and even into breast milk. This makes it possible for an infected mother to pass on the disease to her newborn child, in whom it could present as autism.

Do the numbers stack up? With autism now so widespread, is it likely that so many children-or their mothers-could have been bitten by a relatively uncommon tick?

One answer is that ticks, it appears, are not the only cuplrits. Mosquitoes, fleas and lice may also carry Borrelia (Agric Environ Med, 2002; 9: 257-9), thus vastly increasing the risk of infection. Another theory is that there may be a ‘Borrelia-related complex’ whereinthe bacteria pass unnoticed from generation to generation, and only present when the immune system is under stress. Autistic children are known to suffer from a plethora of autoimmune and metabolic disorders (J Autism Dev Disord, 2000; 30: 475-9), and these could turn latent Borrelia infection into a full-blown attack-with no tick in sight.

Such theories were recently aired at a January 2007 meeting of the newly formed Lyme-Induced Autism Foundation, held in San Diego. Texas physician Dr William Harvey reported that he had many patients who tested positive for Borrelia, and yet, “our part of Texas is not an endemic region of Lyme disease”, he said. “No patient had the typical skin rash, but most had been ill for many years, with similarly ill family members.”

Other delegates agreed. “There may be two forms of Borrelia infection: Lyme disease and epidemic borreliosis-disease spread directly between humans,” said fellow LD physician Dr Radoff. “It is quite possible that the prevalence of autoimmune disorders found in families with autism is an infection that has existed chronically in the body for years, if not decades.”

Dr Warren Levin, another LD practitioner, has reported that, in the 10 children with autism he has seen, all tested positive for Lyme disease.

Predictably, medicine’s knee-jerk reaction to such findings has been to dismiss them, but one group of researchers is taking them seriously. Yet again, that pioneering team of psychiatrists at Columbia University, led by Dr Brian Fallon, has already taken up the challenge and embarked on a huge epidemiological study of Lyme disease and autism.

Fallon believes that two things will emerge from his study: that regions with very high rates of Lyme disease will also have higher-than-normal rates of autism; and that at least some of those autistic children will respond to LD therapy.

“In our work with children with LD, we have encountered a few children with autistic-like disorders,” says Dr Fallon. “When they received intensive antibiotic therapy, the autistic syndromes dramatically improved and, in some cases, resolved.”

Tony Edwards

Stand by for a battle-royal over Alzheimer’s disease (AD)-to take place in
the British High Courts of Justice, no less. Shortly, in a unique court case, NICE (National Institute for Clinical Excellence), the UK’s National Health Service drugs watchdog, will be challenged to defend its decision not to fund Alzheimer’s drugs intended for use in the early stages of the disease.

Ranged on the prosecution benches will be two big guns of the pharmaceutical industry, Pfizer and its marketing arm Eisai, aided and abetted by the Alzheimer’s Society, a vociferous patient support group that equally loudly proclaims itself to have no ties with any drug manufacturers.

What’s all the fuss about? Are the Alzheimer’s drugs any good at all, and are there any alternatives? And what causes the disease in the first place?

Dementia and Alzheimer’s

From near-obscurity only a generation ago, Alzheimer’s disease is now probably, after cancer, the most feared disease of old age. Alzheimer’s has been chillingly described as an affliction whose victims suffer the loss of qualities that define human existence.

Once considered a rare disorder, it is now known to be the most common type of senile dementia, defined as physical damage to the brain in old age that results in major changes to reasoning, memory, personality and behaviour. Until recently, the only way to distinguish Alzheimer’s from other types of dementia was by post-mortem examination of the brain. A typical AD brain is found to be partly atrophied, with the brain cells clumped together in what are called ‘neurofibrillary tangles’ or ‘plaques’.

The second major type of dementia is vascular dementia, where the interruption of the brain’s blood supply, usually due to ‘mini-strokes’, causes brain cells to die. These two main types of dementia can now sometimes be distinguished from each other by brain scans using either magnetic resonance imaging (MRI) or positron-emission tomography (PET).

Senile dementia is not as inevitable as many people might imagine: between 25 and 50 per cent of individuals over 85 are spared it. Nevertheless, dementia is on the increase, so the drug companies claim, because of the simple fact that we’re all living longer. It is believed to be incurable.

Big Pharma’s offerings

Any prolonged chronic illness that is only ended by death is, of course, meat and drink to the pharmaceutical industry. And yet, perhaps surprisingly, there are relatively few drug treat-ments available for Alzheimer’s. First on the market was tacrine (marketed as Cognex) in 1993. Like virtually all of its successors, tacrine is a so-called cholinesterase inhibitor, which acts by artificially maintaining levels of acetyl-choline in the brain. This important brain chemical is known to be reduced by as much as 90 per cent in AD sufferers; it’s also believed to be important for memory, so finding a drug that can preserve the chemical in the brain makes sense.

In fact, the theory is fine-the trouble is the side-effects. After just a decade on the market, tacrine began to be no longer actively marketed after reports of severe liver toxicity. As much as 60 per cent of patients found the drug’s side-effects to be intolerable at high doses. The final nail in tacrine’s coffin was that, after all this, it really doesn’t work (JAMA, 1998; 280: 1777-82).

Since then, three other drugs have come onto the market, all of which attempt to do the same trick of increasing acetylcholine in the brain. As expected, these drugs are all deadly rivals. Pfizer’s Aricept (donepezil), has an advertising tagline that says ‘when Alzheimer’s hits home, Aricept can help’; Novartis’ Exelon (rivastigmine) claims to be ‘another step forward against Alzheimer’s disease’; and Shire Pharmaceuticals/Janssen’s Reminyl (galantamine) sells itself with the somewhat vague tagline ‘Reminyl is now’.

So far, Pfizer is the only manufacturer to have threatened a lawsuit against the recent NICE ruling that none of these drugs is really worth taking in the early stages of AD. Will the drugmaker win their case? Our prediction is no-and, frankly, because the evidence is stacked against them.

The only large-scale, truly independent clinical trial of Pfizer’s Aricept was carried out by a team of British researchers at the University of Birmingham. In a double-blind trial that lasted for more than two years, Aricept was tested head-to-head against a placebo in over 500 patients who had mild-to-moderate AD.

The study’s conclusions? Aricept works, but its benefits are very small-“below minimally relevant thresholds” (Lancet, 2004; 363: 2105-15). As study director Professor Richard Grey stated in the report: “Patients and their families would probably notice no difference if the drug was stopped.”

What’s more, even clinical trials funded by the drug companies them-selves failed to show much benefit with any of their products. For example, Oxford University researchers recently scrutinized data from 24 separate Pfizer-sponsored Aricept trials, involving more than 5000 patients at different stages of AD, and concluded that “the treatment effects are small and are not always apparent in practice”. Add to that the strong likelihood of “many adverse events” such as nausea, vomiting, diarrhoea, muscle cramps, dizziness, fatigue and anorexia, and it’s little wonder that there’s what the researchers politely refer to as a “debate” over whether Aricept is worth a candle (Cochrane Database Syst Rev, 2006; 1: CD001190).

The same Oxford scientists have also examined another of Pfizer’s claims-which is also supported by the strictly independent Alzheimer’s Society-that Aricept helps prevent the onset of AD, stopping what is classified as ‘mild cognitive impairment’ (MCI) from turning into full-blown Alz-heimer’s. The researchers’ conclusion? According to their report: “There is no evidence to support the use of Aricept for patients with MCI. The putative benefits are minor, short-lived and associated with significant side effects” (Cochrane Database Syst Rev, 2006; 3: CD006104).

What of Aricept’s two other rivals, however? Again, independent studies of the clinical data have exposed the drug companies’ marketing hype.

With MCI, for example, Polish researchers concluded earlier this year that the efficacy of all three cholinesterase-blocking drugs was “questionable”, especially given the high incidence of side-effects, some of which-as in the case of Reminyl-apparently can be fatal (Neurol Neurochir Pol, 2007; 41: 13-21).

As for full-blown AD itself, three groups of independent researchers all agree that the three drugs, although having slightly different modes of action, all produce broadly similar effects-or rather, a lack of effects. Their benefit to Alzheimer patients is variously described as “not large” (Cochrane Database Syst Rev, 2006; 1: CD005593), “limited” (Tijdschr Psychiatr, 2006; 48: 17-26) and “small” (Drugs Aging, 2007; 24: 155-67).

Nevertheless, Aricept remains the market leader in a highly profitable $3 billion a year business that is fore-casted to grow exponentially.

But there’s one new drug that is beginning to challenge Aricept. It’s called memantine (marketed as Ebixa, Axura, Namenda and Akatinol). Strictly speaking, it’s not a drug, as it’s derived from the naturally occurring mineral adamantine, and it also works in a different way from its pharmaceutical rivals. Developed by Merz, a German manufacturer of natural health products, the compound appears to protect brain cells against glutamate, the amino acid that is thought to be toxic to the brain in excess amounts and to trigger Alzheimer’s.

Clinical trials of memantine have been promising, showing it to be particularly effective in moderate-to-severe AD, although it generally only slows mental decline rather than reverses it (Drugs, 2006; 66: 1515-34). Detailed testing has found that it appears to benefit attention and information-processing speed more than memory (Int J Geriatr Psychiatry, 2006; Nov 20; epub ahead of print).

Its side-effects are hardly greater than a placebo tablet, with a slight tendency to produce tiredness and dizziness. It is widely used in Germany, often in preference to the standard drugs; however, in Britain, it is still considered experimental.

Alternative treatments

Meanwhile, gradually emerging into the limelight are a number of promising plant-based treatments, some of which turn out to have properties that seem almost tailor-made for AD.

Take the humble culinary sage plant, Salvia officinalis. In addition to having potent antioxidant and anti-inflammatory effects, sage is known to have anticholinergic effects similar to Aricept’s. When tested against placebo in a recent clinical trial, 60 drops of sage oil a day was often found to be better than Aricept at maintaining mental functioning in people with mild-to-moderate AD-and without any side-effects (J Clin Pharm Ther, 2003; 28: 53-9). Sage oil can also improve memory in younger people, too.

Lemon balm (Melissa officinalis) has been found to bind to the brain receptors believed to be involved with anxiety, thus reducing the agitation symptoms seen with AD. Particular strains of the plant have also proved able to slow the decline of mental functioning (Curr Pharm Des, 2006; 12: 4613-23). However, although some proponents recommend these plants as aromatherapy for Alzheimer sufferers, the evidence is considered “inconclusive” (Aust NZ J Psychiatry, 1999; 33: 789-99).

The classic herbal memory-enhancer is Ginkgo biloba, which has been proven in numerous clinical trials to benefit mental faculties in people of all ages. Germany is where it’s most used for Alzheimer’s, as even German conventional doctors consider it prefer-able to the pharmaceutical drugs on offer.

Although it’s by no means a miracle-worker, Ginkgo has been shown to benefit virtually all AD patients to some degree, and about a third of them quite significantly. The recommended dosage is 240 mg/day of the Ginkgo extract codenamed ‘EGb 761’; the benefits normally show up within six months (Pharmacopsychiatry, 2003; 36: 297-303). It’s even been suggested that Ginkgo might help prevent the onset of AD but, so far, no research has been done to test its possible role in Alzheimer’s prevention.

What of the other ‘smart drugs’ that are sometimes claimed to be memory-enhancers for the able-bodied? Of these, only nicergoline (derived from ergot) appears to have any evidence of benefit, with up to a threefold improvement on some performance measures in AD (Cochrane Database Syst Rev, 2001; 4: CD003159). Vinpocetine and piracetam, although better known, don’t appear to have been adequately tested in Alzheimer’s patients to come to any firm conclusions.

On the near horizon, the curry spice curcumin is being investigated as a potential anti-AD compound, after it was recognized that people in India have lower rates of the disease. Lab tests by neurologists at UCLA have already shown that curcumin can repair brain cells damaged by AD, and clinical trials are currently underway
(J Alzheimers Dis, 2006; 10: 1-7).

Traditional Chinese medicine offers two sets of herbal mixtures: Yi-Gan
San is a combination of seven different plants, headed by angelica root; and
Ba Wei Di Huang Wan (BDW) com-prises eight herbs, including cinnamon and peony. Initial research shows that they may be useful in AD (Evidence-Based Complement Altern Med, 2006; 3: 441-5).

There is currently excitement over one Chinese herb in particular, a rare club moss called Huperzia serrata.

Five years ago, an extract of the moss-huperzine alpha (Hup-A)-was tested in more than 200 Chinese diagnosed with mild-to-moderate AD. The results were described as “remarkable”. After taking 400 mcg of Hup-A for less than three months, 60 per cent of the patients were observed to be “clinically on the mend”. Only about a quarter of patients failed to respond. Side-effects were “mild and transient” and, in any case, affected very few of the patients (Zhonghua Yi Xue Za Zhi, 2002; 82: 941-4).

How does Hup-A work? It’s thought to increase acetylcholine levels in the brain. But, in fact, it’s much better than that. It penetrates the brain more effectively than the current drugs, and lasts longer. It also has a wider range of effects, including protecting cells against further damage from inflammation and oxidation (Acta Pharmacol Sin, 2006; 27: 1-26). Here again, a clinical trial is currently ongoing.

The Chinese also use acupuncture for Alzheimer’s, and there is evidence that it may work (Zhongguo Zhen Jiu, 2005; 25: 390-2). In a Westernized variation of this, doctors have tested TENS (transcutaneous electrical nerve stimulation) therapy. Applied to various parts of the body (even the face), TENS has been shown to have some value, particularly in the early stages of AD. However, according to the Japanese doctors using it, the therapy needs to be repeated to sustain benefits beyond six months (Front Med Biol Eng, 2002; 11: 237-47).

Hopeful horizons

One possible AD treatment is chelation therapy. Often derided as mere quackery, chelation has been used for decades by frontier-spirited cardiologists to combat heart disease. The treatment involves transfusing a chemical cocktail into the bloodstream that will bind itself to harmful agents and carry them away. Chelation’s earliest use was to remove toxic levels of lead from workers in the battery and paint industries, but it’s now finding a revival in Alzheimer’s patients.

The argument is this: if metal toxicity is involved in AD, then chelation may be able to bind and flush away the harmful metals before they can cause brain damage.

One of the first trials of chelation used clioquinol as the chelating agent. The results were promising, showing a slight clinical improvement after three weeks (Dement Geriatr Cogn Disord, 2001; 12: 408-14). However, the results of the only subsequent trial were less encouraging (Cochrane Database Syst Rev, 2006; 1: CD005380).

Despite these disappointing findings, a whole slew of researchers across the globe-from Osaka University to Harvard-are actively pursuing the chelation route in hopes of making a breakthrough. Some scientists are even suggesting using ‘nanoparticles’ to trick the brain into allowing more powerful chelating agents past its barriers (Neurosci Lett, 2006; 406: 189-93).

The fact that researchers are being forced to consider such high-tech solutions says two things: the existing treatments aren’t working; and Alzheimer’s may be a rather tougher nut to crack than we thought.

Tony Edwards

However, new research suggests that low-fat milk could actually be doing
us more harm than good, increasing the risk of serious health problems-from infertility to prostate cancer.

Worse, scientists hypothesize that stripping the fat from milk-to make the drink supposedly healthier-could be the very reason for its toxic effects.

Two major studies have discovered that a high-dairy diet increases the risk of prostate cancer-but the real culprit could be the multibillion-pound low-fat industry built upon the belief that animal fats cause heart disease (see WDDTY vol 17 no 11). Scientists now suspect that the real problem is processed, low-fat dairy foods that have been stripped of their protective and health-giving qualities.

The two separate studies-both published in February-have confirm-ed growing suspicions of a link between dairy and prostate cancer. One is the CLUE II study, involving nearly 4000 men in Washington County, Maryland; this found that those who consumed five or more servings a week of dairy foods were more likely to suffer from prostate cancer than those who ate a serving of one or less (Cancer Causes Control, 2007; 18: 41-50).

Similarly, the other study, an analysis of over 29,000 Finnish men taking part in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study), found that the more dairy consumed, the higher the risk of prostate cancer (Int J Cancer, 2007 Feb 2; Epub ahead of print).

These findings deal a double blow to the dairy industry, yet the link between dairy and prostate cancer is not new. As far back as 1975, scientists noted a strong correlation between milk intake and prostate cancer deaths (Am J Clin Nutr, 2005; 81: 1147-54).

Since then, many more reports have confirmed an increased cancer risk from dairy foods-particularly milk, the most common form of dairy consumed.

Initial explanations for such an association blamed saturated dairy fat (Salud Publ Mex, 1997; 39: 298-309), but mounting evidence suggests that the truth could be quite the opposite: that removing the fat from milk may be responsible for the carcinogenic effects.

An American prospective study involving more than 3600 men and 10 years of follow-up-for the first National Health and Nutrition Examination Epidemiologic Follow-up Study (NHEFS)-found that those with the highest intakes of dairy were more than twice as likely to develop prostate cancer than men with the lowest intakes.

However, when the researchers looked at the individual dairy products consumed, they found that the risk was higher only with low-fat milk-and not for whole milk or any other dairy. In fact, whole milk had a slight-albeit statistically not significant-protective effect (Am J Clin Nutr, 2005; 81: 1147-54).

Harvard’s Physicians’ Health Study arrived at a similar conclusion. This study, involving over 20,000 men and 11 years of follow-up, found that the increased risk of prostate cancer associated with dairy intake was attributable primarily to skimmed milk. Of the five dairy foods investigated (milk in cold breakfast cereal, whole milk, skimmed milk, cheese and ice cream), only skimmed milk showed a significantly positive relationship when men consumed one or more servings per day (Am J Clin Nutr, 2001; 74: 549-54).

Similar results were found in a prospective study of more than 25,000 Norwegian men (Int J Cancer, 1997; 73: 634-8) and, in an analysis of milk-drinking and diet in 41 countries, Dr William B. Grant, of the NASA Langley Research Center in Virginia, found that non-fat milk had the highest association with prostate-cancer death rates (Altern Med Rev, 1999; 4: 162-9).

Calcium unbound
Thus, rather than being a healthy choice, low-fat milk-and possibly other low-fat dairy items-may, in fact, be detrimental to men’s health. But why should this be so?

One theory is that removing the fat from milk strips it of certain nutritional components that are vital to health. Fat is found in milk for a reason. It contains vitamins A and D, both of which are necessary for the uptake and use of the calcium and protein elements in milk. Without these vitamins, milk protein and calcium are more difficult to absorb-and can even become toxic to the body.

Calcium, particularly in large amounts, seems to have a specific adverse effect: it suppresses the formation of calcitrol, the hormonal form of vitamin D. Because calcitrol has anticarcinogenic effects on prostate cells, scientists have postulated that a reduction in the amount of calcitrol in the circulation could increase the risk of prostate cancer (Anticancer Res, 1990; 10: 1307-11).

Indeed, a recent study from Harvard showed that a high calcium intake-whether from diet or supplements-was associated with reduced levels of calcitrol and a higher risk of prostate cancer (Cancer Epidemiol Biomarkers Prev, 2006; 15: 203-10). The above-mentioned Finnish study also suggested a connection between calcium and prostate cancer (Int J Cancer, 2007 Feb 2; Epub ahead of print).

While the suppressive effects of calcium from whole milk may be countered by higher levels of vitamin D, such a reversal of calcium effects may not occur with low-fat milk as fat-reduced milk tends to contain little, if any, vitamin D. And even if the vitamin is added to skimmed milk, as it is in the US, it may still be less well-absorbed from fat-reduced milk.

This has been confirmed in studies looking at different types of milk that have shown that calcium from low-fat or skimmed milk is associated with a greater risk of prostate cancer, while calcium from whole milk is not (Am J Clin Nutr, 2005; 81, 1147-54; Am J Clin Nutr, 2001; 74: 549-54).
So, it appears that, far from being good for us, calcium-when separated from the fat in milk-can be toxic to the body.

The CLA connection
Another possible explanation is that stripping the fat from milk also removes other important cancer-protective components such as conjugated linoleic acid (CLA). CLA was identified as a component of milk and dairy products over 20 years ago, and studies have shown it to be a powerful anticarcinogen. In the lab, when human breast and colon cancer cells were bathed in high-CLA milk fat from cows raised on pastureland, the number of cancer cells was reduced by 58 per cent up to 90 per cent (Br J Nutr, 2003; 90: 877-85; Anticancer Res, 2000; 20: 3591-601).

Although modern milking methods and processing affect the CLA content of milk, women who consumed four or more servings a day of high-fat dairy foods were half as likely to develop colorectal cancer as women who ate less than one serving a day; low-fat dairy had no effect. The researchers attributed the results to CLA, although they noted that other potentially anticancer components, such as sphingomyelin and ether lipids, may have also played a role (Am J Clin Nutr, 2005; 82: 894-900).

CLA may protect against prostate cancer by cancelling out the effects of the potentially carcinogenic growth factors found in milk, such as insulin-like growth factor-1 (IGF-1). This occurs naturally-and in identical forms-in both cows and humans. Because cows are milked during and after pregnancy-when growth factors are at their highest-scientists are concerned that consuming milk and dairy could raise IGF-1 levels in humans-perhaps by crossing the gut wall-and trigger an abnormal response leading to, for example, certain cancers.

Indeed, elevated IGF-1 levels have recently been linked to an increased risk of gastrointestinal and breast cancers (Int J Health Serv, 1996; 26: 173-85; Lancet, 1998; 351: 1393-6), lung cancer, childhood cancers, melanoma, and cancers of the pancreas and prostate (Ann NY Acad Sci, 1995; 766: 402-8; J Natl Cancer Inst, 2000; 92: 1910-7).

The association with the prostate appears to be particularly strong. In one study, men with the highest levels of IGF-1 had more than four times the risk of prostate cancer compared with those who had the lowest levels (Science, 1998; 279: 563-6).

Whether the IGF-1 in milk is the real culprit is not yet known. What is clear is that milk stripped of its natural fat is more likely to promote cancer, and the more of its natural fat-and CLA content-that milk retains, the more anticancer benefits it will have.

Infertility
But it’s not only men who are at risk from the hazards of low-fat milk, and the problem isn’t just cancer. Harvard scientists recently confirmed a link between low-fat dairy in the diet and an increased risk of infertility due to lack of egg release-also known as ‘anovulatory infertility’.

This study monitored 18,555 American women aged 24 to 42, without a history of infertility, who were trying to become pregnant or had become pregnant between 1991 and 1999. It showed that women who ate two or more servings of low-fat dairy foods a day, such as skimmed milk or yoghurt, increased their risk of anovulatory infertility by more than 85 per cent compared with women who ate less than one serving of low-fat dairy a week.

Of the low-fat dairy foods, women who consumed one or more servings per week of skimmed or low-fat milk had a significantly higher risk of anovulatory infertility compared with those having less than one serving per week.

In contrast, adding a daily serving of whole milk reduced the risk of infertility by more than 50 per cent. Other high-fat dairy products, such as ice cream, were also associated with a lower risk.

Previous research has suggested that lactose, the sugar found in milk, might be involved in anovulatory infertility, but the present study found no such connection. Instead, the researchers believe that the presence of a fat-soluble substance, which improves ovarian function, might explain the lower risk of infertility from high-fat dairy foods. As with the prostate-cancer studies, there appears to be a substance vital for healthy ovaries that requires the presence of fat for it to be properly absorbed (Hum Reprod, 2007 Feb 28; Epub ahead of print).

This may also explain why studies that have looked at dairy intake and rates of ovarian cancer have found that only low-fat milk and skimmed milk, but not whole milk, were associated with an increased cancer risk. In the Brigham and Women’s Hospital Nurses’ Health Study, based on more than 80,000 women, those who consumed one or more servings of skimmed or low-fat milk daily had a 32-per-cent higher risk of any type of ovarian cancer-and a 69-per-cent higher risk of serous ovarian cancer, the most widespread form-compared with women who had three or fewer servings a month. Whole milk, on the other hand, had no such effect (Int J Cancer, 2004; 110: 271-7).

Similarly, the Iowa Women’s Health Study found that skimmed milk-but not whole milk-was significantly associated with an increased risk of cancer of the ovaries (Am J Epidemiol, 1999; 149: 21-31).

What’s the verdict?
Just as there are often two sides to every story, there are findings that don’t support the ‘low fat = bad, high fat = good’ hypothesis. In one study, for example, whole milk resulted in a threefold increase in ovarian-cancer risk, while low-fat milk reduced the risk (Am J Epidemiol, 1990; 132: 871-6).

These, however, were case-control studies, which are retrospective and, therefore, tend to be less reliable.
Indeed, a recent meta-analysis, which pooled together the data from a number of studies, found that case-control studies on milk and ovarian-cancer risk are conflicting, whereas
the more reliable prospective, cohort studies-which record relevant data before the disease develops-were consistent. And these prospective studies showed that low-fat milk, but not whole milk, was associated with an increased risk of ovarian cancer (Int J Cancer, 2006; 118: 431-41).

Ditching low-fat milk
One of the more worrying elements of these findings is that low-fat milk is so popular. In the Physicians’ Health Study, for instance, skimmed milk was the most-consumed dairy product, accounting for 48 per cent of all dairy (Am J Clin Nutr, 2001; 74: 549-54).
And yet, there are so many reasons to stop drinking the stuff.

As if prostate cancer, infertility and ovarian cancer weren’t bad enough, scientists have also noted a connection between low-fat milk and acne. Taking data again from the Nurses’ Health Study, retrospective evaluation found that women who frequently consumed low-fat dairy such as reduced-fat milk, skimmed milk and cottage cheese as high-school teenagers were more likely to suffer from severe, physician-diagnosed acne at the time.

Skimmed milk showed the strongest association, leading the researchers to speculate that changes in milk composition during the fat-extraction process could aggravate acne. Altering the balance of the hormones in milk, for example, might be an explanation. The addition of whey proteins-added to low-fat and skimmed milk to simulate the consistency of whole milk-could also have a role to play (J Am Acad Dermatol, 2005; 52: 207-14).

The final nail in the coffin, though, is delivered by NASA’s Dr Grant, in his summary of the mounting evidence that non-fat milk is a major player in bringing on heart disease. The report points out that non-fat milk, which contains substantial amounts of dairy protein, is very low in B vitamins. The body’s attempts to metabolize all this protein in the absence of B vitamins contributes to the build up of homocysteine, a known marker for heart disease.

Not surprisingly, Grant’s statistical analysis of the dietary influences on coronary heart disease (CHD) across 32 countries found non-fat milk to have the highest association in men aged 45 and over, and in women aged 75 and over-more than any other dietary factor, including saturated fats (Altern Med Rev, 1998; 3: 281-94).

Evidently, the idea of removing fat from milk to protect the heart is not only putting both men and women at risk from a number of serious health problems, it is also seriously flawed.

The milky way forward
Many researchers are now calling for a revision of current dietary guidelines for dairy intake-which are similar in the US and UK. For example, Dr Jorge Chavarro, research fellow in the Department of Nutrition at Harvard School of Public Health, and lead author of the dairy and infertility study, says that the current dietary guidelines for Americans-that adults consume three or more servings of low-fat milk or equivalent dairy products per day-“may be deleterious for women planning to become pregnant”. His advice to women wanting to conceive is to change their diet. “They should consider changing low-fat dairy foods for high-fat dairy foods; for instance, by swapping skimmed milk for whole milk and eating ice cream, not low-fat yoghurt.”

Considering the other negative health effects linked to low-fat milk, should we all heed this advice?
Sadly, it’s not that simple. While whole milk seems to be a healthier option than low-fat or skimmed milk, it, too, is subjected to processing that destroys some of its nutrients. Pasteurization typically involves heating milk for 30 seconds at 63 degrees C, which destroys beneficial bacteria as well as all the important enzymes that aid milk digestion. Essential vitamins and proteins are also damaged or destroyed.

Homogenization, a process that passes milk through a fine filter, causes other problems by reducing the size
of fat globules by a factor of 10 or more. When protein molecules become attached to these smaller fat globules, this piggy-backing allows the proteins to bypass digestion in the stomach, which may lead to their incomplete digestion and allergies.

Processed milk also contains a host of undesirable components (see box, page 8), which might explain why it’s not just low-fat milk that has been linked to a rash of illnesses, but other sorts of dairy in general.
So, other than avoiding all dairy products altogether, a more sensible option would be to consume milk in its most natural state-raw, unprocessed and full-fat.

Joanna Evans
For more information on raw milk and where you can get it, visit the website: http://www.realmilk.com.