Monthly Archives: August 2015

Estrogen and cognition, with a focus on Alzheimer’s disease.

Aug 20

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One of the reasons to remain on HRT long-term is the benefit to memory and reducing Alzheimer’s disease risk. Alzheimer’s disease: The Cache County memory Study concluded that taking E2 use for more than 10 years reduced the risk of Alzheimer’s disease, if treatment commences at the onset of menopause. Another study found an enduring protective role of endogenous and exogenous E2 on memory in older postmenopausal women. On my web-site under”Menopause recommendations” is the recommendation from the British Menopause Association that using oestregen long term improves cognition. Here is more information of the benefits of oestrogen to the brain. However, to get the benefits the oestrogen must be started soon after menopause begins.
Semin Reprod Med. 2005 May;23(2):172-9.

Estrogen and cognition, with a focus on Alzheimer’s disease.

Pinkerton JV1, Henderson VW.

Author information

Abstract

Cognitive aging is associated with decreases in memory, attention, and visual/motor performance and skills. Dementia consists of loss of memory and other cognitive abilities, associated with social or occupational impairment. Potential neuroprotective effects of estrogen include lowering beta-amyloid, enhancing cholinergic function, promoting synaptic plasticity and nerve process growth, reducing oxidative stress, and enhancing brain glucose transport. Observational and longitudinal studies suggest that hormone therapy may attenuate age-associated cognitive impairment or decrease Alzheimer’s disease but this has not been confirmed by randomized clinical trials. A critical window of time may exist around the menopause when hormone therapy may delay or decrease cognitive changes; however, hormone therapy initiated in the late postmenopause does not improve global cognition and may increase dementia risk.

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The Problem With Prostate Screening

Aug 19

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I was playing golf with a man who had just had a prostate operation. He had 3 biopsies which were all benign, but he had not been able to pass urine normally since then, and had to depend on a permanent catheter and bag. He was in some discomfort. Other men who have had prostate operations often end up with unpleasant complications from the op. Unfortunately, many of them did not need the op as they had benign conditions. So what can men do – proceed with caution. The article below is an eye-opener, which brings me back to another theme I discuss frequently. Scientific fraud and/or obfuscation means we all have to be wary about what we are told by our well-meaning health practitioners on some of these more contentious issues. Mammograms are another example of the same. I hope these blogs I post help you to make the right decisions about your health, in conjunction with your GP. Read my other posts on Prostate screening for more information.

The Problem With Prostate Screening

By RICHARD J. ABLINNOV. 25, 2014

A doctor in Florida performed a robot-assisted prostate surgery. Chris Garlington for The New York Times

TUCSON — SCIENTIFIC data from clinical trials provides the foundation of medical decision making, from a doctor’s prescription pad to sweeping public health policies. Public trust that the data is accurate and unbiased is the glue that binds our $3 trillion health care system. I worry that this trust, particularly when it comes to American men and their physicians and screening programs for prostate cancer, is now at risk.

In 1970 I discovered the prostate-specific antigen, or PSA, which is now the most widely used tool in prostate screenings. But there has been a growing concern about whether the use of the PSA test has led to overdiagnosis and overtreatment, with millions of unnecessary surgeries, complications and deaths.

Nevertheless, the medical community has roundly embraced the results of a recent study finding that PSA screening reduced prostate cancer deaths by 20 percent. The study, the European Randomized Study of Screening for Prostate Cancer, joined another survey, the so-called Swedish Goteborg study (the results of which provided a basis for the European Randomized Study), which found an astounding 44 percent reduction.

But there’s a big problem with both of these studies: In March the Goteborg study’s authors announced in the British Medical Journal that their data “are not available to outside investigators.”

That the researchers would block access to government- and charity-supported research is bad enough. Even worse, it calls into question why, if the data was strong, the researchers wouldn’t open it up to independent scrutiny.

As it turns out, there are some major concerns about the methodology and results of the studies, first raised last fall in the Journal of the National Cancer Institute by two Australian researchers.

The European Randomized Study reported results from seven countries, while Goteborg was a single-site study in Sweden. In both, men were divided into two groups: One underwent regular PSA tests, while the other was not screened. The results were published in The New England Journal of Medicine and the journal Lancet Oncology, respectively.

As the Australian researchers, Ian E. Haines and George L. Gabor Miklos, noticed, there was something strange about the data sets: A large amount of the data in the European Randomized Study came from a separately reported Finnish study, which showed no significant lifesaving benefits of PSA screening.

They found further red flags in terms of biased patient treatment. Many of the men who developed prostate cancer received excessive amounts of a treatment called hormonal monotherapy, which some research now indicates can actually accelerate cancer. Depending on which groups — screened and not screened — those men were in, the results of the study could be significantly compromised. And yet that information was missing from the published reports. When Drs. Haines and Miklos requested the European data to undertake independent analyses, researchers in both studies were unwilling to release it.

Even more troubling was that the European Randomized Study investigators transferred an astounding 60 percent of the data from the Swedish Goteborg study into their own data pool. Since the Goteborg study was alone among country-specific studies in showing an almost 50 percent reduction in prostate cancer deaths for screening recipients, such an overweighting of the data obviously tipped the balance in favor of lives saved. This is a bright-line ethical breach: Without this biased transfer, the lifesaving claims of PSA screening vanish.

Further bias was highlighted by Otis Brawley, the chief medical and scientific officer of the American Cancer Society, and by Paul Goldberg, the editor of the Cancer Letter. They pointed out that the nonscreened Swedish men who contributed to the two studies were not even informed that they were in a clinical trial, which introduced an unacceptable variable between them and the PSA-screened men, who were informed.

Finally, several senior authors of the European trials, and their American supporters, have potential conflicts of interest that relate to payments from companies involved in marketing PSA tests, or in holding patents in the PSA and prostate cancer diagnostic space — relationships documented by the International Committee of Medical Journal Editors, in the forms that accompany the PSA-study publications and in disclosures found in CA: A Cancer Journal for Clinicians.

As a result, those physicians who have not examined the data in depth are now treating patients on the basis of deeply flawed data. How flawed? That’s the real issue: Because the authors won’t release their data, we don’t know.

It is imperative that, as part of America’s continuing efforts at health care reform, we develop a declaration of principles about the need for data transparency. Our regulatory bodies must insist that clinical trials, and especially taxpayer-funded ones, be open to scrutiny by independent investigators who have no ties to industry. Hoarding data, especially flawed data, is unacceptable when lives are at stake.

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Progesterone in Peri- and Postmenopause: A Review.

Aug 19

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Geburtshilfe Frauenheilkd. 2014 Nov;74(11):995-1002.

Progesterone in Peri- and Postmenopause: A Review.

Regidor PA1.

Author information

Abstract

in English, German

Around 14.5 million peri- and postmenopausal women currently live in Germany. Moreover, approximately 450 000 women, each with a life expectancy of around 85 years, reach menopause every year in Germany. The challenge is therefore to find a therapy with few side effects which could improve the quality of life of women with menopausal symptoms. The aim of hormone therapy (HT) is to remedy hormone deficiencies using substances that offer the best trade-off between benefits and risks. This is where progesterone has a new and important role to play. Progesterone is one of the most important gestagens. Biologically effective progesterone formulations created with micronization techniques have been used in clinical practice since 1996. Nevertheless, up until 2003 preference was given to synthetic gestagens rather than progesterone. The increased breast cancer hazard ratio of 1.23 reported in the WHI study and of 2 given in the Million Women Study has been associated with the use of synthetic gestagens. In a comparison between synthetic gestagens and progesterone, the E3N Study showed that the transdermal administration of estrogen and progesterone did not lead to an increase in breast cancer rates (RR: 1.08). The administration of progesterone does not change the HDL/LDL cholesterol ratio. Because of its anti-mineralocorticoid effect, progesterone has no impact on carbohydrate metabolism, hemostasis, blood pressure, thrombogenicity and body weight. The administration of 200 mg/day progesterone over 12 days of a menstrual cycle or a daily administration of 100 mg combined with an estrogen are a safe and well-tolerated option to treat menopausal symptoms, with a better benefit risk profile compared to synthetic gestagens

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More Consensus on Coffee’s Benefits Than You Might Think

Aug 17

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I have been one of those who have advised against coffee intake, as I (erroneously) thought it was harmful. I am glad that the evidence shows otherwise – whoopee – expresso machine, here I come!

See my post of June 8th

Caffeinated coffee lowers risk of breast cancer.

Jun 8

and also in April :

Wake up and smell the coffee … it’s why your cuppa tastes so good

Apr 22

 and more :

This Is Your Brain on Coffee

Jul 22

The New Health Care

More Consensus on Coffee’s Benefits Than You Might Think

MAY 11, 2015

Aaron E. Carroll

When I was a kid, my parents refused to let me drink coffee because they believed it would “stunt my growth.” It turns out, of course, that this is a myth. Studies have failed, again and again, to show that coffee or caffeine consumption are related to reduced bone mass or how tall people are.

Coffee has long had a reputation as being unhealthy. But in almost every single respect that reputation is backward. The potential health benefits are surprisingly large.

When I set out to look at the research on coffee and health, I thought I’d see it being associated with some good outcomes and some bad ones, mirroring the contradictory reports you can often find in the news media. This didn’t turn out to be the case.

Just last year, a systematic review and meta-analysis of studies looking at long-term consumption of coffee and the risk of cardiovascular disease was published. The researchers found 36 studies involving more than 1,270,000 participants. The combined data showed that those who consumed a moderate amount of coffee, about three to five cups a day, were at the lowest risk for problems. Those who consumed five or more cups a day had no higher risk than those who consumed none

Of course, everything I’m saying here concerns coffee — black coffee. I am not talking about the mostly milk and sugar coffee-based beverages that lots of people consume. These could include, but aren’t limited to, things like a McDonald’s large mocha (500 calories, 17 grams of fat, 72 grams of carbohydrates), a Starbucks Venti White Chocolate Mocha (580 calories, 22 grams of fat, 79 grams of carbs), and a Large Dunkin’ Donuts frozen caramel coffee Coolatta (670 calories, 8 grams of fat, 144 grams of carbs).

I won’t even mention the Cold Stone Creamery Gotta-Have-It-Sized Lotta Caramel Latte (1,790 calories, 90 grams of fat, 223 grams of carbs). Regular brewed coffee has 5 or fewer calories and no fat or carbohydrates.

Back to the studies. Years earlier, a meta-analysis — a study of studies, in which data are pooled and analyzed together — was published looking at how coffee consumption might be associated with stroke. Eleven studies were found, including almost 480,000 participants. As with the prior studies, consumption of two to six cups of coffee a day was associated with a lower risk of disease, compared with those who drank none. Another meta-analysis published a year later confirmed these findings.

Rounding out concerns about the effect of coffee on your heart, another meta-analysis examined how drinking coffee might be associated with heart failure. Again, moderate consumption was associated with a lower risk, with the lowest risk among those who consumed four servings a day. Consumption had to get up to about 10 cups a day before any bad associations were seen.

No one is suggesting you drink more coffee for your health. But drinking moderate amounts of coffee is linked to lower rates of pretty much all cardiovascular disease, contrary to what many might have heard about the dangers of coffee or caffeine. Even consumers on the very high end of the spectrum appear to have minimal, if any, ill effects

But let’s not cherry-pick. There are outcomes outside of heart health that matter. Many believe that coffee might be associated with an increased risk of cancer. Certainly, individual studies have found that to be the case, and these are sometimes highlighted by the news media. But in the aggregate, most of these negative outcomes disappear.

A meta-analysis published in 2007 found that increasing coffee consumption by two cups a day was associated with a lower relative risk of liver cancer by more than 40 percent. Two more recent studies confirmed these findings. Results from meta-analyses looking at prostate cancer found that in the higher-quality studies, coffee consumption was not associated with negative outcomes.

The same holds true for breast cancer, where associations were statistically not significant. It’s true that the data on lung cancer shows an increased risk for more coffee consumed, but that’s only among people who smoke. Drinking coffee may be protective in those who don’t. Regardless, the authors of that study hedge their results and warn that they should be interpreted with caution because of the confounding (and most likely overwhelming) effects of smoking.

A study looking at all cancers suggested that it might be associated with reduced overall cancer incidence and that the more you drank, the more protection was seen.

Drinking coffee is associated with better laboratory values in those at risk for liver disease. In patients who already have liver disease, it’s associated with a decreased progression to cirrhosis. In patients who already have cirrhosis, it’s associated with a lower risk of death and a lower risk of developing liver cancer. It’s associated with improved responses to antiviral therapy in patients with hepatitis C and better outcomes in patients with nonalcoholic fatty liver disease. The authors of the systematic review argue that daily coffee consumption should be encouraged in patients with chronic liver disease.

The most recent meta-analyses on neurological disorders found that coffee intake was associated with lower risks of Parkinson’s disease, lower cognitive decline and a potential protective effect against Alzheimer’s disease (but certainly no harm).

A systematic review published in 2005 found that regular coffee consumption was associated with a significantly reduced risk of developing Type 2 diabetes, with the lowest relative risks (about a third reduction) seen in those who drank at least six or seven cups a day. The latest study, published in 2014, used updated data and included 28 studies and more than 1.1 million participants. Again, the more coffee you drank, the less likely you were to have diabetes. This included both caffeinated and decaffeinated coffee.

Is coffee associated with the risk of death from all causes? There have been two meta-analyses published within the last year or so. The first reviewed 20 studies, including almost a million people, and the second included 17 studies containing more than a million people. Both found that drinking coffee was associated with a significantly reduced chance of death. I can’t think of any other product that has this much positive epidemiologic evidence going for it.

I grant you that pretty much none of the research I’m citing above contains randomized controlled trials. It’s important to remember that we usually conduct those trials to see if what we are observing in epidemiologic studies holds up. Most of us aren’t drinking coffee because we think it will protect us, though. Most of us are worrying that it might be hurting us. There’s almost no evidence for that at all.

If any other modifiable risk factor had these kind of positive associations across the board, the media would be all over it. We’d be pushing it on everyone. Whole interventions would be built up around it. For far too long, though, coffee has been considered a vice, not something that might be healthy.

That may change soon. The newest scientific report for the U.S.D.A. nutritional guidelines, which I’ve discussed before, says that coffee is not only O.K. — it agrees that it might be good for you. This was the first time the dietary guideline advisory committee reviewed the effects of coffee on health.

There’s always a danger in going too far in the other direction. I’m not suggesting that we start serving coffee to little kids. Caffeine still has a number of effects parents might want to avoid for their children. Some people don’t like the way caffeine can make them jittery. Guidelines also suggest that pregnant women not drink more than two cups a day.

I’m also not suggesting that people start drinking coffee by the gallon. Too much of anything can be bad. Finally, while the coffee may be healthy, that’s not necessarily true of the added sugar and fat that many people put into coffee-based beverages.

But it’s way past time that we stopped viewing coffee as something we all need to cut back on. It’s a completely reasonable addition to a healthy diet, with more potential benefits seen in research than almost any other beverage we’re consuming. It’s time we started treating it as such.

Aaron E. Carroll is a professor of pediatrics at Indiana University School of Medicine. He blogs on health research and policy at The Incidental Economist, and you can follow him on Twitter at @aaronecarroll.

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I am Moving.

Aug 17

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The practice I work at has been sold. It will close in the middle of Sept. I am in the process of looking for somewhere nearby that will suit my style of practice. As soon as I have more details I will post it on my Web-site. All those who have made appointments will be notified of the changes. Anyone who has trouble finding me, check my web-site, or ask the compounding chemist you use for my new address and telephone number. They will know.

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Statins Vs Garlic – which is better for your heart?

Aug 16

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Coronary Calcium Score Benefits of Aged Garlic.

Dr Jeffrey Dach

Posted on June 12, 2015

Garlic_CAlcium_Score_Basket_WikimediaCoronary Calcium Score Benefits of Aged Garlic

How to Reduce Calcium Scores  ?

Jim has an elevated coronary calcium score in the 95% percentile indicating high risk for future heart attack.  He is being treated by his cardiologist with daily aspirin and atorvastatin (lipitor), a statin drug to reduce cholesterol.

Currently we are following a number of similar patients with elevated coronary calcium score treated with statin drugs by their cardiologist.  The elevated calcium score indicates higher risk for future coronary event such as chest pain, angina, heart attack etc.  Current cardiology dogma dictates treatment with statin drugs to lower cholesterol, thus preventing heart disease.

Cholesterol Theory has Been Falsified

The problem with this cardiology dogma is the cholesterol theory of atherosclerotic disease has been falsified by many studies which are summarized nicely by Dr. William R Ware from the University of Ontario.  Dr Ware’s fine article in Medical Hypotheses 2009, reveals there is no correlation between serum cholesterol and the amount of atherosclerotic plaque when reviewing either autopsy studies or coronary calcium score studies.(9)  Thus, the theory that elevated cholesterol  causes atherosclerotic plaque is essentially falsified.

Coronary Artery CalcificationStatin Drugs Disappointing for Calcium Score

Two randomized trials using statin drugs to reduce calcium scores showed  disappointing results.(10,11) Left Image CAT scan showing calcified coronary artery (yellow arrow).

In Dr. Houslay’s trial published in Heart 2006, 102 patients were randomized and treated for two years with either 80 mg/d atorvastatin (lipitor) or placebo.(10)  As expected, the statin treated group had a 53% reduction in LDL cholesterol, while the placebo group had no change in theirs.  The researchers were expecting benefit from the statin treatment.  They found the opposite.  Paradoxically, the statin group had greater increase in calcium score (26%) than the placebo group (only 18%).  The authors concluded:“statin treatment does not have a major effect on the rate of progression of coronary artery calcification.”(10)

The second trial by Dr Schmermund in Circulation 2006 randomized 471 patients with no pre-existing coronary artery disease, treated for one year with either  low dose (10mg/d) or high dose (80 mg/d) atorvastatin therapy.  In the high dose group (80 mg/d) the LDL cholsterol was reduced from 106 to 87 mg/dL (approximately 20% reduction).  However, the low dose statin  group  had no change in LDL cholesterol from baseline (108 vs 109 mg/dL).   The authors were expecting reduction in progression of calcium score in the high dose statin group with a 20% reduction in LDL cholesterol.  They were surprised to find no difference in calcium scores between the two groups.  The high dose atorvastatin group actually had slightly greater progression of calcium score (27%) vs (25%) for the low dose group.  The authors concluded,”Coronary artery calcification (CAC) progression showed no relationship with on-treatment LDL cholesterol levels.”  (11)

According to Dr. Gill in a 2010 report: as of the year 2010 there had been five randomized controlled studies showing that statin drug treatment does not reduce coronary calcium score.  Worse, the statin treatment showed progression of coronary calcium score indistinguishable from the non-treated placebo group.

matthew j budoff md calcium score garlicWhat Interventions Have Been Successful in Reduced Calcium Score ?

As we can see from the above studies, statin drugs are quite effective for lowering cholesterol, yet fail to reduce or slow progression of calcium score.  Again, this provides even more evidence falsifying the cholesterol theory of atherosclerotic heart disease.  Perhaps we should look elsewhere for a treatment modality in the patient with elevated calcium score. Left image courtesy of Matthew J Budoff MD and OCWeekly Magazine.

Dr. Matthew J Budoff did just this, exploring the use of Aged Garlic in retarding progression of calcium score in three studies. (1-3)

In the first study published in 2006 Journal of Nutrition, twenty three “high risk” patients maintained on a stable dose of statin drug and aspirin were randomized to either placebo or 4 mL of Aged Garlic (1200 mgKYOLIC Aged Garlic Liquid) After one year of treatment, the Aged Garlic group showed a 7.5 %progression of calcium score, considerably lower than the 22.2% progression in the placebo group. (1) Remember that both groups were maintained on statin drugs during the one year study.

In the second study by Dr Budoff published in Preventive Medicine 2009, sixty five “intermediate risk” patients, all maintained on statins,  were randomized and treated for one year with either placebo or Aged Garlic Extract (250 mg). (2)  In addition, the garlic group was vitamins: Vitamin B12 (100 microg), folic acid (300 microg),Vitamin B6 (12.5 mg) and l-arginine (100 mg) . (The product used was: Kyolic 108 Aged Garlic by Wakunaga) After one year of treatment, the Aged Garlic Group had significantly less Coronary Artery Calcification progression (6.8%)  compared to the placebo group (26.5%). (see Table 2, Budoff Preventive Medicine 2009).     In addition the Garlic Group had “favorable improvement in oxidative biomarkers and vascular function”(1)

Budoff_Aged_Garlic_CAC_Fig 2_2006Left Image: Fig 2 showing Aged Garlic Group left and placebo right.  Aged Garlic Group(left bars) shows lower progression of calcium score (blue bar), reduction in IgG IgM MDA LDL, IC/apoB oxidative bio-markers and reduction in Homocysteine (red bar) compared to placebo (right). Courtesy of Aged garlic extract retards progression of atherosclerosis Budoff Preventive medicine 2009 .

A third study by Dr Matt Budoff  in the 2012 Journal of Cardiovascular Research randomized 65 firefighters to one year treatment with either Aged Garlic plus Co-Q-10 (Kyolic Aged Garlic-Co-Q10 Formula 110, Wakunaga ) or to placebo. (3)  Some were taking statin drugs. About 25% of the Aged Garlic+CoQ10 were on statins, compared to 31% of placebo group were on statins.

Table One Budoff 2012 Aged Garlic CoQ10 Calcium Score Firefighters_JCDRAfter one year of treatment the aged Garlic group showed less progression of calcium score (32 vs. 58 absolute) and (18.9% vs 27.4%).  CRP was also lower in the Garlic group.  See Left Image :Table One courtesy Budoff 2012 (3).

Additional Benefits of Garlic

In a 2013 study by  Dr. Kumar, Garlic was found beneficial as an adjunct to Metformin 500 mg twice a day (BID) in obese diabetics.(12)  Garlic lowers blood pressure has been found useful in hypertensive patients.(13) In addition, Garlic has anti-microbial properties and has uses as an anti-microbail agent (4-8).

Garlic Reduces Calcium Score Progression, Mechanism of Action

My previous article discussed the failure of the cholesterol hypothesis, and recent revelations about atherosclerotic plaque as infected biofilm, and the association with increased gut permeability, also called “Leaky Gut”.   This would certainly explain our somewhat paradoxical findings in the three studies by Dr Matthew Budoff showing Garlic more effective than statin drugs.  A natural antimicrobial agent, the lowly Garlic bulb, shows ability to retard progression of calcium score while the high and mighty statin drug fails,  even though cholesterol is reduced.

Garlic as Anti-Microbial

Although various mechanisms have been proposed to explain the benefits of Garlic in cardiovascular disease, I would like to concentrate on Garlic as an anti-microbial agent.(4-8)  Unlike conventional antibiotics which may disrupt the normal intestinal flora, Garlic’s antimicrobial properties act against pathogenic gut bacteria with relative sparing of the beneficial, “friendly” gut bacteria.(4)   Dr Bayan in 2014 says: “garlic exerts a differential inhibition between beneficial intestinal microflora and potentially harmful enterobacteria”(4)   Dr Rees studied Garlic’s antimicrobial activity finding broad spectrum activity against  “many  bacteria, yeasts, fungi and virus. All microorganisms tested were susceptible to garlic.”(5)  Dr Filocamo in 2012 studied Garlic in a bacterial population representative of the colonic microbiota.   Lacto-baccillus was more resistant to Garlic compared to the Clostridial which was was more susceptible.   The author suggested the “consumption (of garlic) may favor the growth of these beneficial bacterial species in the gut. Garlic intake has the potential to temporarily modulate the gut microbiota.”(6)  A full discussion of the antimicrobial spectrum of Garlic can be found in an excellent article in 2015 by Dr Packia Lekshmi (7) Mark Slevin’s  2012 article  reported on natural products with vascular protective properties and significant anti-atherogenic potential.  Dr Slevin mentions Aged Garlic, Resveratrol and Green Tea extract (ECGC ) as the most promising (8)

Pseudomonas BioFilm in Atherosclerotic Plaque Material

Dr Bernard Lanter studied athersclerotic plaque specimens, identifying Pseudomonas 16S rRNA genes in 6 of 15 cases, indicating colonization by Pseudomonas biofims. (14) The virulence of Pseudomonas is attributed to Quorum Sensing, the ability of the bacterial cells to communicate with one another to form Bio-Films. (16) Dr. Bjarnsholt considers disruption of this Quorum Sensing to be the key to controlling Psudomonas Biofilm infections.  That is exactly what Garlic does.  In Vitro and In Vivo animal studies show Garlic inhibits quorum sensing and virulence of Pseudomonas. (15)  An excellent way to study the effect of Allicin, the active ingredient in Garlic, on the PSeudomonas organism is to tag the bacteria with the Green Flourscent Protein (GFP).  This was done published in the 2013 with an elegant series of in-vitro experiemnts using Allicin treated GFP-modified Pseudomonas organisms.(17) Dr. Lihua’s group showed that:

“Allicin treatment not only reduced the adhesion ratio of P. aeruginosa, but also inhibited EPS (extracellular polysaccharide) secretion and down-regulates production of some Quorum Sensing -controlled virulence factors.  These results imply that allicin can disturb the formation and
maturation of P. aeruginosa biofilm, and suggest that allicin may represent a promising therapeutic candidate for the management of P. aeruginosa biofilms.”(17)

Poly-Microbial Colonization

Others have found diverse colonies of bacterial, fungal and protozoal life-forms colonizing biofilms in atherosclerotic plaque specimens (18-20),  In view of this,  investigating other botanical agents with known antimicrobial activity might also be useful, such as Olive Leaf extract, Oregano Oil, Berberine, etc.   Perhaps a combination of such natural products would have a more powerful synergistic effect. Other natural anti-microbials such as colloidal silver, and Iodine should be considered as well.   This would be a fertile area for future research.

Our program for Elevated Calcium Score:

Aged Garlic,
Co-Q-10,
L-Arginine
Reveratrol, Pterostilbene
Homocysteine reducing program (B6, B12, Methylfolate)
LinusPauling Protocol (Lysine, Proline, Vitamin C, Tocotrienols)
William Davis Track Your Plaque Protocol (Niacin, Omega-3 Fish Oil, Vitamin D3, Vitamin K2, Eliminate Wheat products)
Weight Reduction,
Hormone Optimization (optimize thyroid, testosterone, estrogen progesterone)
Heal the Leaky Gut (Probiotics, Glutamine, Colostrum)
Eliminate NSAIDS, PPI’s which cause dysbiosis and leaky gut.
Eliminate Pesticides,  Glyphosate and GMO food, eat Organic.

Articles With related Interest:

Atherosclerotic Plaque as Infected Biofilm

Preventing Heart Attacks with Ouabain

Thyroid Pills Prevent Heart Attacks

How to Reverse Heart Disease with the Coronary Calcium Score

Heart Disease Vitamin C and Linus Pauling

Jeffrey Dach MD
7450 Griffin Road Suite 180
Davie FL 33314
954-792-4663
www.jeffreydachmd.com

Links and References

1) http://jn.nutrition.org/content/136/3/741S.full
Budoff, Matthew. “Aged garlic extract retards progression of coronary artery calcification.” The Journal of nutrition 136.3 (2006): 741S-744S. Aged garlic extract retards progression of atherosclerosis Budoff Preventive medicine 2009

2) http://www.ncbi.nlm.nih.gov/pubmed/19573556
Budoff, M. J., et al. “Aged garlic extract supplemented with B vitamins, folic acid and L-arginine retards the progression of subclinical atherosclerosis: a randomized clinical trial.” Preventive medicine 49.2-3 (2009): 101.
Previous studies demonstrated that aged garlic extract reduces multiple cardiovascular risk factors. This study was designed to assess whether aged garlic extract therapy with supplements (AGE+S) favorably affects inflammatory and oxidation biomarkers, vascular function and progression of atherosclerosis as compared to placebo.
METHODS: In this placebo-controlled, double-blind, randomized trial (conducted 2005-2007), 65 intermediate risk patients (age 60+/-9 years, 79% male) were treated with a placebo capsule or a capsule containing aged garlic extract (250 mg) plus Vitamin B12 (100 microg), folic acid (300 microg), Vitamin B6 (12.5 mg) and l-arginine (100 mg) given daily for a 1 year. All patients underwent coronary artery calcium scanning (CAC), temperature rebound (TR) as an index of vascular reactivity using Digital Thermal Monitoring (DTM), and measurement of lipid profile, autoantibodies to malondialdehyde (MDA)-LDL, apoB-immune complexes, oxidized phospholipids (OxPL) on apolipoprotein B-100 (OxPL/apoB), lipoprotein (a) [Lp (a)], C-reactive protein (CRP), homocysteine were measured at baseline and 12 months. CAC progression was defined as an increase in CAC>15% per year and an increase in TR above baseline was considered a favorable response.
RESULTS: At 1 year, CAC progression was significantly lower and TR significantly higher in the AGE+S compared to the placebo group after adjustment of cardiovascular risk factors (p<0.05). Total cholesterol, LDL-C, homocysteine, IgG and IgM autoantibodies to MDA-LDL and apoB-immune complexes were decreased, whereas HDL, OxPL/apoB, and Lp (a) were significantly increased in AGE+S to placebo.
CONCLUSION: AGE+S is associated with a favorable improvement in oxidative biomarkers, vascular function, and reduced progression of atherosclerosis.

3) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425023/
Zeb, Irfan, Budoff M  et al. “Aged Garlic Extract and Coenzyme Q10 Have Favorable Effect on Inflammatory Markers and Coronary Atherosclerosis Progression: A Randomized Clinical Trial.” Journal of Cardiovascular Disease Research 3.3 (2012): 185–190. PMC. Web. 11 June 2015.
Aged garlic extract (AGE) and coenzyme Q10 (CoQ10) have been shown to affect multiple cardiovascular risk factors. The current study evaluates the effect of AGE combined with CoQ10 on inflammatory markers and progression of coronary atherosclerosis compared with placebo.
Methods and Results: In this placebo-controlled, double-blind, randomized trial, 65 intermediate risk firefighters (age 55 ± 6 years) were treated with a placebo capsule or a capsule containing AGE and CoQ10 (AGE+CoQ10, 1200 and 120 mg, respectively) daily for 1 year. All participants underwent coronary artery calcium (CAC) scanning and C-reactive protein (CRP) at baseline and at 12 months. At 1 year, mean CAC progression was significantly lower in AGE+CoQ10 (32 ± 6 vs. 58 ± 8, P = 0.01) than placebo. Similarly, CRP were significantly decreased in AGE+CoQ10 compared with placebo (-0.12 ± 0.24 vs. 0.91 ± 0.56 mg/L, P < 0.05). After adjustment for age, gender, conventional cardiac risk factors, and statin therapy, AGE+CoQ10 was associated with 3.99 fold (95% 1.3–12.2, P = 0.01) lack of CAC progression compared with the placebo.

4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4103721/
Bayan, Leyla, Peir Hossain Koulivand, and Ali Gorji. “Garlic: A Review of Potential Therapeutic Effects.” Avicenna Journal of Phytomedicine 4.1 (2014): 1–14. Print.
It has been documented that garlic exerts a differential inhibition between beneficial intestinal microflora and potentially harmful enterobacteria

5) http://www.ncbi.nlm.nih.gov/pubmed/24420031/
World J Microbiol Biotechnol. 1993 May;9(3):303-7. doi: 10.1007/BF00383068.
A quantitative assessment of the antimicrobial activity of garlic (Allium sativum).
Rees LP1, Minney SF, Plummer NT, Slater JH, Skyrme DA.
An aqueous extract of freeze-dried garlic (Allium sativum), when incorporated into growth media, inhibited many representative bacteria, yeasts, fungi and a virus. All microorganisms tested were susceptible to garlic. Quantitative assessment of the minimum inhibitory concentrations for bacteria and yeasts showed values ranging from 0.8 to 40.0 mg garlic ml(-1). Fungal radial colony growth was inhibited by at least 25% at concentrations as low as 2.0 mg garlic ml(-1). The 50% endpoint neutralization titre for rotavirus was 2.4 to 2.8 μg ml(-1). Lactic acid bacteria were the least sensitive microorganisms to the inhibitory effects of garlic. In mixed culture studies of Lactobacillus acidophilus and Escherichia coli, garlic prevented the establishment of E. coli, although the final outcome of competition was not affected.

6) http://www.ncbi.nlm.nih.gov/pubmed/22480662
Filocamo, Angela, et al. “Effect of garlic powder on the growth of commensal bacteria from the gastrointestinal tract.” Phytomedicine 19.8 (2012): 707-711.
Garlic (Allium sativum) is considered one of the best disease-preventive foods. We evaluated in vitro the effect of a commercial garlic powder (GP), at concentrations of 0.1% and 1% (w/v), upon the viability of representative gut bacteria. In pure culture studies, Lactobacillus casei DSMZ 20011 was essentially found to be resistant to GP whereas a rapid killing effect of between 1 and 3 log CFU/ml reduction in cell numbers was observed with Bacteroides ovatus, Bifidobacterium longum DSMZ 20090 and Clostridium nexile A2-232. After 6h incubation, bacterial numbers increased steadily and once the strains became resistant they retained their resistant phenotype upon sub-culturing. A colonic model was also used to evaluate the effect of GP on a mixed bacterial population representing the microbiota of the distal colon. Lactic acid bacteria were found to be more resistant to GP compared to the clostridial members of the gut microbiota. While for most bacteria the antimicrobial effect was transient, the lactobacilli showed a degree of resistance to garlic, indicating that its consumption may favour the growth of these beneficial bacterial species in the gut. Garlic intake has the potential to temporarily modulate the gut microbiota.

7) Antimicrobial Spectrum Allium Garlic Packia Lekshmi 2015
Packia Lekshmi, N. C. J., et al. “Antimicrobial Spectrum of Allium Species–A Review.” History 15.44 (2015): 1-5.

8) pdf vascular protective supplements anti_atherosclerotic Slevin Mark Vasc Cell 2012  .  Slevin, Mark, et al. “Unique vascular protective properties of natural products: supplements or future main-line drugs with significant anti-atherosclerotic potential.” Vasc Cell 4.1 (2012): 9.

9) cholesterol atherosclerosis falsified coronary artery plaque Ware Medical Hypotheses 2009 Ware, William R. “The mainstream hypothesis that LDL cholesterol drives atherosclerosis may have been falsified by non-invasive imaging of coronary artery plaque burden and progression.” Medical hypotheses73.4 (2009): 596-600.

10)  Houslay, E S et al. “Progressive Coronary Calcification despite Intensive Lipid‐lowering Treatment: A Randomised Controlled Trial.” Heart 92.9 (2006): 1207–1212. PMC. Web. 11 June 2015.
To evaluate the effect of intensive lipid‐lowering treatment on coronary artery calcification in a substudy of a trial recruiting patients with calcific aortic stenosis.
Methods In a double blind randomised controlled trial, 102 patients with calcific aortic stenosis and coronary artery calcification were randomly assigned by the minimisation technique to atorvastatin 80 mg daily or matched placebo. Coronary artery calcification was assessed annually by helical computed tomography.
Results 48 patients were randomly assigned to atorvastatin and 54 to placebo with a median follow up of 24 months (interquartile range 24–30). Baseline characteristics and coronary artery calcium scores were similar in both groups. Atorvastatin reduced serum low density lipoprotein cholesterol (−53%, p < 0.001) and C reactive protein (−49%, p < 0.001) concentrations whereas there was no change with placebo (−7% and 17%, p > 0.95 for both). The rate of change in coronary artery calcification was 26%/year (0.234 (SE 0.037) log arbitrary units (AU)/year; n  =  39) in the atorvastatin group and 18%/year (0.167 (SE 0.034) log AU/year; n  =  49) in the placebo group, with a geometric mean difference of 7%/year (95% confidence interval −3% to 18%, p  =  0.18). Serum low density lipoprotein concentrations were not correlated with the rate of progression of coronary calcification (r  =  0.05, p  =  0.62).
Conclusion In contrast to previous observational studies, this randomised controlled trial has shown that, despite reducing systemic inflammation and halving serum low density lipoprotein cholesterol concentrations, statin treatment does not have a major effect on the rate of progression of coronary artery calcification.

11)  Schmermund, Axel, et al. “Effect of Intensive Versus Standard Lipid-Lowering Treatment With Atorvastatin on the Progression of Calcified Coronary Atherosclerosis Over 12 Months A Multicenter, Randomized, Double-Blind Trial.” Circulation 113.3 (2006): 427-437.

Background— Recent clinical trials have suggested that intensive versus standard lipid-lowering therapy provides for additional benefit. Electron-beam computed tomography provides the opportunity to quantify the progression of coronary artery calcification (CAC) in serial measurements.
Methods and Results— In a multicenter, randomized, double-blind trial, 471 patients (age 61±8 years) who had no history of coronary artery disease and no evidence of high-grade coronary stenoses (>50% diameter reduction) were randomized if they had ≥2 cardiovascular risk factors and moderate calcified coronary atherosclerosis as evidenced by a CAC score ≥30. Patients were assigned to receive 80 mg or 10 mg of atorvastatin per day over 12 months. Progression of CAC volume scores could be analyzed in 366 patients. After pretreatment with 10 mg of atorvastatin for 4 weeks, 12 months of study medication reduced LDL cholesterol from 106±22 to 87±33 mg/dL in the group randomized to receive 80 mg of atorvastatin (P<0.001), whereas levels remained stable in the group randomized to receive 10 mg (108±23 at baseline, 109±28 mg/dL at the end of the study, P=NS). The mean progression of CAC volume scores, corrected for the baseline CAC volume score, was 27% (95% CI 20.8% to 33.1%) in the 80-mg atorvastatin group and 25% (95% CI 19.1% to 30.8%) in the 10-mg atorvastatin group (P=0.65). CAC progression showed no relationship with on-treatment LDL cholesterol levels.

12) Kumar, Rahat et al. “Antihyperglycemic, Antihyperlipidemic, Anti-Inflammatory and Adenosine Deaminase– Lowering Effects of Garlic in Patients with Type 2 Diabetes Mellitus with Obesity.” Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 6 (2013): 49–56. PMC. Web. 12 June 2015.

13) Xiong, X. J., et al. “Garlic for hypertension: A systematic review and meta-analysis of randomized controlled trials.” Phytomedicine 22.3 (2015): 352-361.

14) Lanter, Bernard B., Karin Sauer, and David G. Davies. “Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture.” MBio 5.3 (2014): e01206-14.

15) Harjai, K., R. Kumar, and S. Singh. “Garlic blocks quorum sensing and attenuates the virulence of Pseudomonas aeruginosa.” FEMS immunology and medical microbiology 58.2 (2010): 161.

16) Bjarnsholt, Thomas, and Michael Givskov. “The role of quorum sensing in the pathogenicity of the cunning aggressor Pseudomonas aeruginosa.” Analytical and bioanalytical chemistry 387.2 (2007): 409-414.
Lihua, Lin, et al. “Effects of allicin on the formation of Pseudomonas aeruginosabiofinm and the production of quorum-sensing controlled virulence factors.” Pol J Microbiol 62 (2013): 243-51.

18)  Ott, Stephan J., et al. “Detection of diverse bacterial signatures in atherosclerotic lesions of patients with coronary heart disease.” Circulation 113.7 (2006): 929-937.

19) Ott, S. J., et al. “Fungal rDNA signatures in coronary atherosclerotic_Ott_2007_Athrosclerosis Fungal rDNA signatures in coronary atherosclerotic plaques.” Environmental microbiology 9.12 (2007): 3035-3045.

20)  Putative biofilm-forming organisms in the human vasculature: expanded case reports and review of the literature. Stephen Eugene Fry, Jeremy Eugene Ellis, Matthew Andrew Shabilla, Delyn Lorene Martinez, Renatta Schwarz, Richard Heuser, Constantine Moschonas . Phlebological Review 2014; 22, 1: 24–37 Biofilm_forming organisms human vasculature Stephen Eugene Fry Phlebological Review 2014

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Aug 16

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Emma, our 2 month old grandchild, became seriously ill at the end of last week. SHe was rushed into Canberra Hospital with suspected Meningitis. The doctors, including one of the best paediatricians in Canberra, were unable to do a lumbar puncture, in spite of repeated attempts. They were unable to keep a drip up, again, after many efforts. The parents were distraught, so Doriann and I flew down on Sat. to give support and help. Doriann had her prayer group and Mothers Union pray for Emma, which was a few hundred people. She turned the corner rapidly and was looking much better by the time we got to Canberra. She is a tough little fighter.

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Testosterone for Dry Eye

Aug 13

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Dry eyes (Gritty, irritable eyes) are common as we get older. Menopausal women in particular suffer from it (unless they are seeing me and getting testosterone in their scripts). I have discussed the benefits of testosterone for women over the last few years, especially for improving libido, energy, memory, osteoporosis and reducing the breast cancer risk. Here is another good reason for menopausal women to take testosterone.
Testosterone for Dry Eyes Jeffrey Dach MD
Meibomian Gland Testosterone for Dry EyesTestosterone
for Dry Eye Syndrome

by Jeffrey Dach MD

Mrs. B was 58 years old with typical menopausal symptoms of night sweats and hot flashes, and came to see me because of dry itchy, red eyes.  The lids sometimes swell because of the irritation.  Over the years, Mrs B had been to numerous eye doctors who gave her various drops to lubricate the eye, antibiotic drops and steroid drops.  She has been given instructions for cleaning and irrigating the eyes.  The eye drops seem to help somewhat but the irritation always returns whenever she stops them.  Lately, the condition is getting worse and nothing seems to help.

Above left image: courtesy of wikimedia commons, red arrow points to meibomian glands in edge of eye lid which secrete oil which lubricates the eye.

Low Testosterone Level

A routine hormone panel showed that Mrs B had low hormone levels, and her testosterone level was especially low. I explained to Mrs B that her dry eye syndrome was caused by low testosterone levels, and testosterone would help.

Cured With Testosterone, Surely You Must Be Joking, Doctor

Six week later, after starting her testosterone as sublingual drops, Mrs B reported her eyes were much better.  She also started a complete bioidentical hormone program. Mrs B’s ophthalmologist, Dr H, was an old friend of mine and we would occasionally attend the same social functions.   At one of these social functions, Dr H approached to say that a patient (no name) reported that I had cured her dry eyes with testosterone, and surely you must be joking, Doctor.  His gesture and facial expression with his eyes rolling back were quite distinctive.

Testosterone for Dry Eyes

in the Opthalmology Medical Literature

Apparently, Dr H is unaware of the supportive evidence in his own specialty medical journals.  We will look at a few of these supportive articles that recommend testosterone for evaporative dry eye syndrome.  About 5 million Americans have Dry Eye Syndrome caused by dysfunction of the lubricating glands, which are called the lacrimal and meibomian glands.  The small glands at the upper outer eye are the lacrimal glands, and the meibomian glands are located in the eye lid at the upper and lower edges (see diagram below).

Tears in the Lacrinmal System Testosterone Dry EyesLeft Image :Tear system: a. tear gland / lacrimal gland, b. superior lacrimal punctum, c. superior lacrimal canal, d. tear sac / lacrimal sac, e. inferior lacrimal punctum, f. inferior lacrimal canal,  g. nasolacrimal canal.

Dr David A Sullivan and Dry Eye Research

Much of the research on testosterone and dry eyes has been done by David A Sullivan at Schepens Eye Research Institute at Harvard Medical School.(4)

Dr Sullivan Research in Mouse Model Of Sjogren’s

Dr. Sullivan’s early work in the 1990’s involved Sjogrens syndrome, and the discovery that women with Sjögren’s syndrome are androgen-deficient causing meibomian gland dysfunction, tear film instability, and the evaporative dry eye characteristic Sjogren’s, which is an autoimmune disorder. (1)  Sullivan published a study in 1991 which showed that testosterone inhibited the progression of autoimmune disease in the lacrimal glands mice with Sjogren’s. His mouse model of Sjogren’s showed that the testosterone suppressed the magnitude of lymphocyte infiltration in the lacrimal gland 22- to 46-fold.(6)

Lacrimal and Meibomian Glands Regulated by Testosterone

In a 1999 report, Sullivan suggested that androgens (testosterone) regulate both lacrimal and meibomian gland function, and suggest that eye drops containing testosterone may be safe and effective treatment for dry eyes in Sjögren’s syndrome.(1)

Chalazion of the Meibomian Gland, Testosterone for Dry EyesLeft Image: Chalazion, obstructed, infected meibomian gland upper eye lid.  This image is useful to give you an idea of where the glands are locared in the lid.  There are 20 – 30 small Meibomian glands located along the edge of the upper and lower lid that secrete oil which lubricates the surface of the eye.  When one becomes obstructed, it swells up and is called a Chalazion. Treatment is to relieve the obstruction and allow drainage. Courtesy of wikimedia commons.

Men on Testosterone Blockers Get Dry Eyes

In 2000,  Dr Sullivan reported that men taking testosterone blockers have dry eye syndrome.  Men on testosterone blocker drug treatment for prostate cancer were found to had poor quality of tear fluid.  This was demonstrated by analyzing the meibomian gland secretions.  Their dry eye symptoms included light sensitivity, painful and blurry eyes.  Sullivan said,”the use of anti-androgen pharmaceuticals was associated with significant changes in the relative amounts of lipids in meibomian gland secretions. Our findings indicate that chronic androgen deficiency is associated with meibomian gland dysfunction and dry eye.” (2)

In 2001, Drs Worda and Nepp from Vienna Austria reported that topically administered androgen can restore the lipid phase of the tear film, and was useful in treatment of keratoconjunctivitis sicca, medical terms for Dry Eyes. (3)

Complete Insensitivity to Androgen and Dry Eyes

Next, Dr Sullivan turned his attention to a genetic disorder called Complete Insensitivity to Androgen (CIAS).  In this genetic disorder, the androgen receptor is nonfunctional, and subsequently, there is insensitivity to testosterone.  Without a functioning receptor, the normal activity of testosterone is completely blocked.

Dr Sullivan examined the tears (ie. Meibomian gland secretions), in women with CIAS and compared them to normal controls.  The patients with CIAS had alteration in the lipid fractions of tear fluid, ( ie meibomian gland secretions). This study was published in a 2002 report in Arch Ophthalmology (5).

Trans-Dermal Testostorone For Dry Eye Syndrome

In 2003, DrConnor reported transdermal testosterone is safe and effective treatment for dry eye, with the post-menopausal females having the greatest relief of symptoms. (10)

Molecular Biology Mouse Studies of Gene Expression

In 2005, Dr Schirra et al studied the molecular biology of testosterone, and gene expression in the meibomian gland of mice. Dr Schirra reported that testosterone regulates the expression of more than 1500 genes in the mouse meibomian gland which serves to stimulate lipid and fatty acid metabolism in the lubricating eye fluid.
(11)

The Evidence is Overwhelming

The sum total of the above evidence is overwhelming that testosterone playes a key role in production of oil, the lipid component for lubricating the eyes, and that testosterone deficiency is a treatable cause of dry eye syndrome.  The treatment is testosterone, a bioidentical hormone.

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Testosterone treatment for low sex drive in naturally menopausal women:

Aug 12

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Testosterone treatment for women has been hotly debated. My experience, and the evidence, is that it not only helps libido, but is good for energy, vitality and cognition (memory) as well. If you search “testosterone for women” on my website, you will find interesting evidence for this. This is another study that confirms this.
Climacteric. 2010 Apr;13(2):121-31. doi: 10.3109/13697131003675922.

Testosterone treatment of HSDD in naturally menopausal women: the ADORE study.

Panay N1, Al-Azzawi F, Bouchard C, Davis SR, Eden J, Lodhi I, Rees M, Rodenberg CA, Rymer J, Schwenkhagen A, Sturdee DW.

Author information

Abstract

OBJECTIVE:

To evaluate the efficacy and safety of a transdermal testosterone patch (TTP, 300 microg/day) in naturally menopausal women with hypoactive sexual desire disorder (HSDD).

METHODS:

A total of 272 naturally menopausal women, predominantly not using hormone therapy, were randomized in this 6-month, placebo-controlled, double-blind, multicenter study to receive twice weekly either TTP or an identical placebo. Efficacy endpoints measured were the 4-week frequency of satisfying sexual episodes (SSE) using the Sexual Activity Log, the sexual desire domain of the Profile of Female Sexual Function and distress by the Personal Distress Scale. Safety was assessed by adverse events, laboratory parameters and hormone levels.

RESULTS:

The TTP group demonstrated significant improvements in SSE (p = 0.0089) as well as in sexual desire (p = 0.0007) and reduced personal distress (p = 0.0024) versus placebo at 6 months (intent-to-treat analysis, n = 247). The results were significant for all three endpoints in the subgroup (n = 199) not using hormone therapy. Similar numbers of women treated with placebo and TTP discontinued (n = 39, 27.5% vs. n = 26, 20%), reported adverse events (including application site reactions) (n = 101, 71.1% vs. n = 81, 62.3%) and withdrew due to adverse events (n = 20, 14.1% vs. n = 9, 6.9%). No clinically relevant changes were noted in laboratory parameters. Serum free and total testosterone levels increased from baseline in the TTP group (geometric means 5.65 pg/ml and 67.8 ng/dl, respectively, at week 24) within the physiological range; no changes were seen in estradiol and sex hormone binding globulin levels.

CONCLUSIONS:

TTP was effective in treating HSDD and improving sexual function in this study of naturally menopausal women with and without concurrent hormone therapy.

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Why does hair change colour and turn grey?

Aug 12

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16 March 2015, 2.26pm AEDT

Health Check: why does hair change colour and turn grey?

Most of us find our first “greys” by the time we turn 30, usually at the temples, then later, across the scalp.

Men generally have more grey hairs than women. crumpart/Flickr, CC BY-NC

Most of us find our first “greys” by the time we turn 30, usually at the temples, then later, across the scalp. While many people find the salt and pepper look appealing, others go to great lengths to conceal these locks.

The grey hair “rule of thumb” is that by the age of 50, half of the population have lost the colour in 50% of their hair. When researchers tested this rule, they found that 74% of people aged between 45 and 65 had grey hair, with an average intensity of 27%.

Generally, men have more grey hair than women. Asians and Africans have less grey hair than Caucasians.

What determines the colour of hair?

Hair colour is produced by cells known as melanocytes, which migrate into the hair bulb as the hair follicles develop in utero. The melanocytes produce pigment that is incorporated into the growing hair fibres to produce hair in a bewildering array of natural shades.

Hair colour depends on the presence and ratios of two groups of melanins: eumelanins (brown and black pigments) and pheomelanins (red and yellow pigments). While variations in the ratio of these pigments can produce an large number of colours and tones, siblings often have strikingly similar hair colour.

Hair colour varies according to body site, with eyelashes being darkest because they contain high levels of eumalanin. Scalp hair is usually lighter than pubic hair, which often has a red tinge, due to the presence of more phaeomelanin pigments. A red tinge is also common in underarm and beard hair, even in people with essentially brown hair on their scalp.

Hormones such as melanocyte-stimulating hormone can darken light hair, as can high levels of oestrogen and progesterone, which are produced in pregnancy. Certain drugs such as those to prevent malaria can lighten hair, while some epilepsy medications can darken it.

Siblings often have strikingly similar hair colour. hans905/Flickr, CC BY-NC-SA

Blond children tend to see their hair darken around the age or seven or eight. The mechanism for this is unknown and probably not related to hormones, as the darkening precedes puberty by a number of years.

New parents often find the first coat of their baby’s hair is darker than expected. It is not until this first hair is shed and replaced, at around eight to 12 months of age, that you get a clear indication of their hair colour.

Growth

Human hair growth is cyclical. During the anagen phase, hair grows continuously at a rate of 1cm per month. Anagen can last three to five years on the scalp and produce hair that grows to between 36 to 60cm in length.

At the end of the anagen phase, the follicle turns off, hair growth stops and remains off for the three months. Towards the end of this resting (telogen) phase, the hair is shed and the follicle remains empty until the anagen phase of the cycle restarts.

Pigment production also turns on and off in rhythm with the hair cycle. When pigment cells turn off at the end of one hair cycle and fail to turn back on with the onset of the next, hair becomes grey.

Losing colour

Genetic factors appear to be important in determining when we turn grey. Identical twins seem to go grey at a similar age, rate and pattern, however we’re yet to identify the controlling genes.

There is no evidence to link the onset of greying to stress, diet or lifestyle. Certain autoimmune diseases such as vitiligo and alopecia areata can damage pigment cells and induce greying. However, these conditions are uncommon and can explain only a tiny fraction of greying.

Don’t worry, stress won’t turn your hair grey. frankieleon/Flickr, CC BY

Early greying occurs in premature ageing syndromes such as Hutchinson’s-progeria and Werner syndrome, where every aspect ageing in the body is accelerated. Premature greying can also be seen in people affected by pernicious anaemia, autoimmune thyroid disease or Down syndrome.

So, why doesn’t pigment production turn back on?

At the end of each hair cycle, some pigment-producing melanocytes become damaged and die. If the melanocyte stem cell reservoir at the top of the hair follicle can replenish the bulb, this keeps pigment production going. But when the reservoir of stem cells is exhausted, pigment production stops and the hair turns grey.

Scientists have long known that in order to prevent hair from going grey they would need to either prolong the life of the melanocytes in the hair bulb – by protecting them from injury – or expand the melanocyte stem cell reservoir in the upper or top region of the hair follicle so they continue to replace lost pigment cells.

A group of French scientists have identified a new series of agents that protect hair follicle melanocytes from damage at the end of the hair cycle. This enables pigment production to restart as soon as the next hair cycle begins.

The agents work by mimicking the action of an enzyme called DOPAchrome tautomerase. This enzyme is the naturally occurring antioxidant in the hair bulb that protects melanocytes from oxidative damage. By duplicating the effects of DOPAchrome tautomerase, melanocyte metabolism and survival improves.

The new agents are being formulated into a product that can be applied as a spray-on serum or shampoo. But they won’t re-colour grey hair or bring back the dead cells that produce hair colour. Instead, they protect your melanocytes.

So for those who cannot find it within themselves to embrace the salt and pepper look, new options are on the horizon.

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