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Showing posts with label Dr William R. Davis. Show all posts
Showing posts with label Dr William R. Davis. Show all posts

Tuesday, November 12, 2013

Testosterone and the Heart Part Two - Dach

Testosterone and the Heart Part Two by Jeffrey Dach MD



In Part One, we discussed a 2010 study from Boston University in which testosterone was given to immobilized, elderly, obese male smokers.  The study was halted early because of poor outcome with increased heart attacks and “cardiac events”  in the testosterone treated group.

Second Study Shows  Poor Outcome in Testosterone Group

A second study from the University of Texas was just published in JAMA .(2)  This study was done on Veterans undergoing coronary angiography with documented coronary artery disease.  Some of these Veterans had low testosterone levels (below 300) .  These veterans were given testosterone treatment and followed.  At the end of three years of follow up, the untreated men had a  20%  incidence of stroke,  heart attack or death, while the testosterone treated group had a higher 26% incidence.  This is 20% untreated, vs. 26% treated.  Clearly, the testosterone did not miraculously reverse the atherosclerosis disease in this group of veterans.(2-6)

Benefits of Testosterone Clearly Documented in Medical Literature

As discussed in part one, decades of research studies have shown that low testosterone in men is a risk factor for early mortality from cardiovascular disease, and testosterone treatment reduces mortality, especially in the diabetic males. (7-10)

Testosterone Treatment Does Not Reverse Heart Disease

However, it is clear from these two studies that testosterone by itself is insufficient as a therapy to reverse coronary artery plaque in men who have diets and lifestyles which promote heart disease, and who already have significant underlying coronary artery disease.

Track Your Plaque BlogLeft Image logo courtesy of Track Your Plaque Blog.

Track Your Plaque Program

For our office patients who are interested in reversing coronary artery plaque, we use the William Davis MD Track Your Plaque Program. This is an excellent program which is well thought out.  See my article on this: Reversing Heart Disease.


I wonder what the outcome of these two studies would have been if the testosterone treated group had been started on the Track Your Plaque Program which monitors lipo-protein profile and the Calcium Score, and uses diet and lifestyle modification and supplements to reduce Calcium Score and increase LDL particle size.

There are many unanswered questions.  I also  wonder what the Vitamin D levels were, and what the thyroid levels were on these men,   How much trans fats were they consuming?  How much were they smoking and how much alcohol did they consume?  How much overweight were they?

Conclusion

One conclusion seems clear and that is testosterone by itself does not replace the Track Your Plaque Program of Diet, Lifestyle modification and Supplements to reverse heart disease.  As these two studies show, clinical outcomes for Testosterone Treatment may actually be worse for subgroups of men with severe coronary artery disease, especially when no changes are made to the diet and lifestyles that promote heart disease.

Jeffrey Dach MD
7450 Griffin Road, Suite 180/190
Davie, Florida 33314
954-792-4663
www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com

Articles With Related Content:

Low Testosterone Diagnosis and Treatment
HCG in Males with Low Testosterone
Testosterone Benefits, PSA and Prostate Part One
Testosterone and PSA Part Two
Clomid for Men with Low Testosterone Part One
Low Testosterone From Pain Pills
Low Testosterone Associated with Increased Mortality
Testosterone Reduces Mortality
Testosterone Blockade Increases Mortality
Testosterone Found Beneficial For Diabetes

Links and References:
(1)http://www.ncbi.nlm.nih.gov/pubmed/20592293
N Engl J Med. 2010 Jul 8;363(2):109-22. Epub 2010 Jun 30.
Adverse events associated with testosterone administration.
Basaria S, Coviello AD, Travison TG, Storer TW, Farwell WR, Jette AM, Eder R, Tennstedt S, Ulloor J, Zhang A, Choong K, Lakshman KM, Mazer NA, Miciek R, Krasnoff J, Elmi A, Knapp PE, Brooks B, Appleman E, Aggarwal S, Bhasin G, Hede-Brierley L, Bhatia A, Collins L, LeBrasseur N, Fiore LD, Bhasin S. Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine and Boston Medical Center, Boston, Massachusetts 02118, USA.

2) http://jama.jamanetwork.com/article.aspx?articleID=1764051  Association of Testosterone Therapy With Mortality, Myocardial Infarction, and Stroke in Men With Low Testosterone Levels  by Rebecca Vigen, MD, MSCS1; Colin I. O’Donnell, MS2,3; Anna E. Barón, PhD2,3; Gary K. Grunwald, PhD2,3; Thomas M. Maddox, MD, MSc2,3,4; Steven M. Bradley, MD, MPH2,3,4; Al Barqawi, MD3; Glenn Woning, MD3; Margaret E. Wierman, MD2,3; Mary E. Plomondon, PhD2,3,4; John S. Rumsfeld, MD, PhD2,3,4; P. Michael Ho, MD, PhD2,3,4  The University of Texas at Southwestern Medical Center, Dallas 2VA Eastern Colorado Health Care
JAMA. 2013;310(17):1829-1836.

3) http://health.clevelandclinic.org/2013/11/concerns-raised-about-testosterone-therapy/  Concerns Raised about Testosterone Therapy Study: testosterone replacement linked to heart risks By Steven Nissen, MD | 11/8/13 2:26 p.m.
4) Testosterone treatments linked with heart riskshttp://www.thetowntalk.com/viewart/20131112/LIFESTYLE/311130006/Testosterone-treatments-linked-heart-risks
5) http://online.wsj.com/news/articles/SB10001424052702303661404579180294201174958  Testosterone Therapy Tied to Heart Risks
Veterans With History of Heart Disease Had Higher Risk of Death, Heart Attack and Stroke, According

6) http://www.latimes.com/science/sciencenow/la-sci-heart-disease-testosterone-replacement-20131105,0,3592717.story  Testosterone medication may boost risk of heart attack, stroke, death
7) http://www.ncbi.nlm.nih.gov/pubmed/22496507  J Clin Endocrinol Metab. 2012 Jun;97(6):2050-8. doi: 10.1210/jc.2011-2591. Epub 2012 Apr 11.  Testosterone treatment and mortality in men with low testosterone levels. Shores MM, Smith NL, Forsberg CW, Anawalt BD, Matsumoto AM.
Source  Veterans Affairs Puget Sound Health Care System, 1660 South Columbian Way, S-116PES, Seattle, Washington 98108, USA.

8) http://www.endocrine-abstracts.org/ea/0025/ea0025p163.htm
Endocrine Abstracts (2011) 25 P163
Low testosterone predicts increased mortality and testosterone replacement therapy improves survival in men with type 2 diabetes
Vakkat Muraleedharan1,2, Hazel Marsh1 & Hugh Jones1,2

9) http://www.ncbi.nlm.nih.gov/pubmed/23999642
Eur J Endocrinol. 2013 Oct 21;169(6):725-33. doi: 10.1530/EJE-13-0321. Print 2013.
Testosterone deficiency is associated with increased risk of mortality and testosterone replacement improves survival in men with type 2 diabetes.
Muraleedharan V, Marsh H, Kapoor D, Channer KS, Jones TH.
Source  Robert Hague Centre for Diabetes and Endocrinology, Barnsley Hospital NHSFT, Gawber Road, Barnsley S75 2EP, UK.

Jeffrey Dach MD
7450 Griffin Road, Suite 180/190
Davie, Florida 33314
954-792-4663
www.jeffreydach.com
www.drdach.com
www.naturalmedicine101.com
www.truemedmd.com
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Read the complete article here.

Tuesday, October 16, 2012

CT heart scans and radiation: The real story

 
CT heart scans and radiation: The real story “My personal opinion is that many patients today who are receiving multiple CT scans may well be getting at least comparable doses to subjects that have now developed malignancies from x-ray radiation received in the 1930s and '40s. And, similar to those days when the doses were unknown, the dose that patients receive today over a course of years of multiple CT scans is also completely unknown . . .

“I recommend that all healthcare providers become familiar with the concept that 1 in 1000 CT studies of the chest, abdomen, or pelvis may result in cancer.”

Richard C. Semelka, MD
Professor and Vice Chairman, Department of Radiology
University of North Carolina–Chapel Hill

Is this just hype to generate headlines? Or is the truth buried in the enormous marketing clout of the medical device industry, among which the imaging device manufacturers reign supreme?
It’s been over 110 years since radiation was first used for medical imaging. Over those years, it has had its share of misadventures.

In the 1930s and 1940s, before the dangers of radiation were recognized, shoe shoppers had shoes fitted using an x-ray device of the foot to assess fit. High doses of radiation were used to shrink enlarged tonsils and extinguish overactive thyroid glands. Attitudes towards radiation were so lax that doctors commonly permitted themselves to be exposed without protection day after day, year after year, until an unexpected rise in blood cancers like leukemia was observed. As recently as the 1970s and 1980s, cancers like Hodgkins’ disease were treated with high doses of radiation, also leading to radiation-induced diseases decades later.

Not all radiation is bad. Radiation can also be used as a therapeutic tool and even today remains a useful and reasonably effective method to reduce the size, sometimes eliminate, certain types of cancer. Forty percent of people with cancer now receive some form of radiation as part of their treatment (Ron E 2003).

Just how much does medical radiation add to our exposure?  Estimates vary, but most experts estimate that medical imaging provides approximately 15% of total lifetime exposure. In other words, radiation exposure from medical imaging is simply a small portion of total exposure that develops over the years of life. Exposure can be much higher, however, in a specific individual who undergoes repeated radiation imaging or treatment of one sort or another.

For all of us, exposure to medical radiation is part of lifetime exposure from multiple sources, added to the radiation we receive from the world around us. Just by living on earth, we are exposed to radiation from space and naturally-occurring radioactive compounds, and receive somewhere around 3.0 mSv per year (U.S. Nuclear Regulatory Commission). (Doses for radiation exposure are commonly expressed in milliSieverts, mSv, a measure that reflects whole-body radiation exposure.) People living in high-altitude locales like Colorado get exposed to an additional 30–50% ambient radiation (1.0–1.5 mSv more per year).

Much of the information on radiation exposure comes from studies like the Life Span Study that, since 1961, has tracked 120,000 Japanese exposed to radiation from the atomic bombs dropped in 1945 (Preston DL et al 2003). Although regarded as a high-dose exposure study for obvious reasons, there are actually thousands of people in this study who were exposed to lesser quantities of radiation (because of distance from the bomb sites) who still display a “dose-response” increased risk for cancer many years later in life. Radiation exposures of as little as 5–20 mSv showed a slight increase in lifetime risk.

Occupational and excessive medical exposure to radiation also provides a “laboratory” to examine radiation risk. Miners exposed to radon gas; patients exposed to the imaging agent, Thorotrast, containing radioactive isotope thorium dioxide and used as an x-ray contrast agent in the 1930s and 1940s and possesses the curious property of lingering in the body for over 30 years after administration; radium injections administered between 1945 and 1955 to treat diseases like ankylosing spondylitis and tuberculosis, all provide researchers an opportunity to study the long-term effects of various types of radiation exposure over many years (Harrison JD et al 2003).

The excess exposure of workers and several hundred thousand nearby residents to the Mayak nuclear plant in Russia has also revealed a “dose-response” relationship, with increasing exposure leading to more cancers, including leukemia and solid cancers of the bone, liver, and lung (Shilnikova NS et al 2003). Nuclear waste released into the Techa river between 1948 and 1956 contaminated drinking water used by over 100,000 Russians. A plant explosion in 1957 also released an excess of radiation into the atmosphere, yielding exposure via inhalation.

Some sources estimate that at least 272,000 people have been affected by radiation from the Mayak plant. This unfortunate situation has, however, yielded plenty of data on radiation exposure and its long-term effects.

It’s also been known for several decades that people who receive therapeutic radiation for treatment of cancer, even with the reduced doses now employed, are subject to increased risk of a second cancer consequent to the radiation treatment.

From experiences like this, radiation experts estimate that an exposure of 10 mSv increases a population’s risk for cancer by 1 in 1000 (Semelka RC et al 2007).

This question was recently thrust into the spotlight with publication of a study from Columbia University in New York suggesting that a 20-year old woman would be exposed to a lifetime risk of cancer as high as 1 in 143 consequent to the radiation received during a CT coronary angiogram. (Important note: This was estimated risk from a CT coronary angiogram, not a simple heart scan that we advocate for the Track Your Plaque program.) The risk at the low end of the spectrum would be in an 80-year old man (because of the shorter period of time to develop cancer), with a risk of 1 in 5017. If “gating” to the EKG is added (which many scan centers do indeed perform nowadays), risk for a 60-year old woman is estimated at 1 in 715; risk for a 60-year old male, 1 in 1911 (Einstein AJ et al 2007). This study generated some criticism, since it did not directly involve human subjects, but used “phantoms” or x-ray dummies to simulate x-ray exposure. Nonetheless, the point was made: CT coronary angiograms in current practice do indeed expose the patient to substantial quantities of radiation, sufficient to pose a lifetime risk of cancer.

The media frenzy  The NY Times ran an article called With Rise in Radiation Exposure, Experts Urge Caution on Tests in which they stated:

"According to a new study, the per-capita dose of ionizing radiation from clinical imaging exams in the United States increased almost 600 percent from 1980 to 2006. In the past, natural background radiation was the leading source of human exposure; that has been displaced by diagnostic imaging procedures, the authors said."

“This is an absolutely sentinel event, a wake-up call,” said Dr. Fred A. Mettler Jr., principal investigator for the study, by the National Council on Radiation Protection. “Medical exposure now dwarfs that of all other sources.”

Radiation is a widely used imaging tool in medicine. Although CT scans of the brain, bones, chest, abdomen, and pelvis account for only 5% of all medical radiation procedures, they are responsible for nearly 50% of medical radiation used. It’s been known for years that increasing radiation exposure increases cancer risk over many years, but the boom of newer, faster devices that provide more detailed images has opened the floodgates to expanded use of CT scanners.

But before we join in the hysteria, let's first take a look at exposure measured for different sorts of tests:

Typical effective radiation dose values for common tests

Computed Tomography
Head CT 1 – 2 mSv
Pelvis CT 3 – 4 mSv
Chest CT 5 – 7 mSv
Abdomen CT 5 – 7 mSv
Abdomen/pelvis CT 8 – 11 mSv
Coronary CT angiography 5 – 12 mSv

Non-CT
Hand radiograph Less than 0.1 mSv
Chest radiograph Less than 0.1 mSv
Mammogram 0.3 – 0.6 mSv
Barium enema exam 3 – 6 mSv
Coronary angiogram 5 – 10 mSv
Sestamibi myocardial perfusion (per injection) 6 – 9 mSv
Thallium myocardial perfusion (per injection) 26 – 35 mSv
Source: Cynthia H. McCullough, Ph.D., Mayo Clinic, Rochester, MN  A plain, everyday chest x-ray, providing less than 0.1 mSv exposure, provides about the same quantity of radiation exposure as flying in an airplane for four hours, or the same amount of radiation from exposure to our surroundings for 11–12 days. Similar exposure arises from dental x-rays.

If you have a heart scan on an EBT device, then your exposure is 0.5-0.6 mSv, roughly the same as a mammogram or several standard chest x-rays.

With a heart scan on a 16- or 64-slice multidetector device, exposure is around 1.0-2.0 mSv, about the same as 2-3 mammograms, though dose can vary with this technology depending on how it is performed (gated to the EKG, device settings, etc.)

CT coronary angiography presents a different story. This is where radiation really escalates and puts the radiation exposure issue in the spotlight. As Dr. Cynthia McCullough's chart shows above, the radiation exposure with CT coronary angiograms is 5-12 mSv, the equivalent of 100 chest x-rays or 20 mammograms. Now, that's a problem.

The exposure is about the same for a pelvic or abdominal CT. The problem is that some centers are using CT coronary angiograms as screening procedures and even advocating their use annually. This is where the alarm needs to be sounded. These tests, as wonderful as the information and image quality can be, are not screening tests. Just like a pelvic CT, they are diagnostic tests done for legitimate medical questions. They are not screening tests to be applied broadly and used year after year.

It’s also worth giving second thought to any full body scan you might be considering. These screening studies include scans of the chest, abdomen, and pelvis. These scans, performed for screening, expose the recipient to approximately 10 mSv of radiation (Radiological Society of North American, 2007). Debate continues on whether the radiation exposure is justified, given the generally asymptomatic people who generally undergo these tests.

Always be mindful of your radiation exposure, as the NY Times article rightly advises. However, don't be so frightened that you are kept from obtaining truly useful information from, for instance, a CT heart scan (not angiography) at a modest radiation cost.

Heart scans, CT coronary angiograms and the future  Unfortunately, practicing physicians and those involved in providing CT scans are generally unconcerned with radiation exposure. The majority, in fact, are entirely unaware of the dose of radiation required for most CT scan studies and unaware of the cancer risk involved. It is therefore up to the individual to insist on a discussion of the type of scanner being used, the radiation dose delivered (at least in general terms), the necessity of the test, alternative methods to obtain the same diagnostic information, all in the context of lifetime radiation exposure.

Our concerns about radiation exposure all boil down to concern over lifetime risk for cancer, a disease that strikes approximately 20% of all Americans. Many factors contribute to cancer risk, including obesity, excessive saturated fat intake, low fiber intake, lack of vitamin D, repeated sunburns, excessive alcohol use, smoking, exposure to pesticides and other organochemicals, asbestos and other industrial exposures, electromagnetic wave exposure, and genetics. Radiation is just one source of risk, though to some degree a controllable one.

Some people, on hearing this somewhat disturbing discussion, refuse to ever have another medical test requiring radiation. That’s the wrong attitude. It makes no more sense than wearing lead shielding on your body 24 hours a day to reduce exposure from the atmosphere. Taken in the larger context of life, radiation exposure is just one item on a list of potentially harmful factors.

It is, however, worth some effort to minimize radiation exposure over your lifetime, particularly before age 60, and by submitting to high-dose testing only when truly necessary, or when the potential benefits outweigh the risks. Thus, with heart scans and CT coronary angiography, some thought to the potential benefits of knowing your score or the information gained from the CT angiogram need to be considered before undergoing the test. Often the practical difficulty, of course, is that your risk for heart disease simply cannot be known until after the test.

In our view, in the vast majority of instances a simple CT heart scan can serve the simple but crucial role of quantifying risk for heart attack and atherosclerotic plaque. CT heart scans yield this information with less than a tenth of the radiation exposure of a CT coronary angiogram. In people without symptoms and a normal stress test, there is rarely a need for CT coronary angiography with present day levels of radiation exposure. Perhaps as technology advances and the radiation required to generate images is reduced, then we should reconsider.

Early experiences are suggesting that the newest 256-slice scanners, now being developed but not yet available, will cut the dose exposure of 64-slice CT angiograms in half (from 27.8 mSv to 14.1 mSv in a recent Japanese study). The 256-slice scanners will allow scanning that is faster over a larger area in a given period of time.

Thankfully, the scanner manufacturers are increasingly sensitive to the radiation issue and have been working on methods to reduce radiation exposure. However, it still remains substantial.

References: Einstein AJ, Henzlova MJ, Rajagopalan S. Estimating risk of cancer associated with radiation exposure from 64-slice computed tomography coronary angiography. JAMA 2007 Jul 18;298(3):317–323.
Harrison JD, Muirhead CR. Quantitative comparisons of cancer induction in humans by internally deposited radionuclides and external radiation. Int J Radiat Biol 2003 Jan;79(1):1–13.
Hausleiter J, Meyer T, Hadamitzyky M et al. Radiation Dose Estimates From Cardiac Multislice Computed Tomography in Daily Practice: Impact of Different Scanning Protocols on Effective Dose Estimates. Circulation 2006;113:1305–1310.
Kalra MK, Maher MM, Toth TL, Hamberg LM, Blake MA, Shepard J, Saini S. Strategies for CT radiation dose optimization. Radiology 2004;230:619–628.
Mayo JR, Aldrich J, Müller NL. Radiation exposure at chest CT: A statement of the Fleischner Society. Radiology 2003; 228:15–21.
Mori S, Nishizawa K, Kondo C, Ohno M, Akahane K, Endo M. Effective doses in subjects undergoing computed tomography cardiac imaging with the 256-multislice CT scanner. Eur J Radiol 2007 Jul 10; [Epub ahead of print].
Preston DL, Pierce DA, Shimizu Y, Ron E, Mabuchi K. Dose response and temporal patterns of radiation-associated solid cancer risks. Health Phys 2003 Jul;85(1):43–46.
Ron E. Cancer risks from medical radiation. Health Phys 2003 Jul;85(1):47–59.
Shilnikova NS, Preston DL, Ron E et al. Cancer mortality risk among workers at the Mayak nuclear complex. Radiation Res 2003 Jun;159(6):787–798.
Semelka RC, Armao DM, Elias J Jr, Huda W. Imaging strategies to reduce the risk of radiation in CT studies, including selective substitution with MRI. J Magn Reson Imaging 2007 May;25(5):900–9090.

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Sunday, October 14, 2012

Results of my second serial CAC Scan just in.

I have been working hard on slowing plaque growth for several years but mostly in the last year and a half because I had my first viable CAC scan to provide a measuring point baseline for reference.

Other comments on the report follow.
  • IMPRESSION: Stable exam compared to Sept 15, 2011

  • PATIENT: 69 year old man with no cardiac symptoms but a past history of cardiovascular disease resulting in 6 MI events over a 17 year period. His current stress level is low. He has a history of prior cardiac procedures including CABG (1x), Angiography and Coronary Stent (3x). He has a family history of stroke and heart disease in a first or second degree relative.

  • YOUR AGATSTON CALCIUM SCORE IS: 1072.3

  • Your current EBT heart was compared to your most recent prior scan and the progression of calcified plaque is less than 15% annually. This is a very good result and is consistent with a low risk for coronary event over the next few years.

Encouraging but no resting on my laurels. The 22% annualized plaque growth in the RCA is a matter of concern reminding me that further improvement is necessary so adjustments may have to be made in my diet etc.


Prior Scan was Sept 15, 2011
Current Scan Oct 5, 2012
My assessment is that it looks pretty good except for % change on LMCA and the RCA
That line below the chart that ends with 4% is good.
Have consult with doctor tomorrow (10/15/2012). Stay tuned for a more qualified analysis.




Note my treatment plan which seems to be paying off is that of the Track Your Plaque Program. It primarily consists of diet and supplements with minimal drug intervention (especially 'no statins' which I do not tolerate). It includes advanced lipid analysis then treating atherogenic ones such as Lp(a) and apo B or LDL particle number and particle size.

Wednesday, September 26, 2012

It's the Calcium Score Stupid! - HeartHawk

My Photo

Tuesday, November 23, 2010

JUPITER to Earth: It's the Calcium Score Stupid!
Well, well, well! A funny thing happened on the way to the "statin forum." Astra-Zeneca, in a bald-faced attempt to broaden the market for its statin product Crestor, ended up proving beyond a shadow of a doubt that heart scans and calcium scoring is the most powerful predictor of heart attacks in asymptomatic people.

A post hoc analysis of the MESA study population using JUPITER criteria revealed at 25-fold increase in risk for persons having a positive calcium score. These two studies were fairly large so it was adequately powered to deliver results with a high degree of confidence.

For years docs like Bill Davis and Bill Blanchet have been screaming this from the hilltops and it something every Track Your Plaque practitioner knows. If you have a positive calcium score you have coronary artery disease and your risk of a heart attack skyrockets. Fortunately, it also gives you often decades of warning so you can actually DO something about it. Coupled with technologies like advanced lipoprotein you can find the root causes and correct them.

So, "thank you" Atra-Zeneca. I know you did it for the money - but what the heck - you might end up having helped save some lives in spite of it!

Now darn it, go out talk to your doc about getting that heart scan if you have any doubts about having the seeds of heart disease in your arteries.

Looking out for your health,
---


Who is HeartHawk?
I am a numbers guy, an engineer, MBA, and for the real numbers geeks, a Six Sigma Black Belt (statistics on steroids). I am also a heart disease sufferer. It took my mother, her brother, and their father. One minute they were alive and symptom free, the next they were dead. No good-byes, just gone. So, I became a heart health activist and resolved that I will die some other way. This blog is about my journey to save myself and others, unearthing advances and atrocities, separating hope from hype, and delivering the unvarnished truth about curing heart disease, both good and bad. So, hold on tight. I promise you a hell of a ride!

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Read HeartHawk's blog here.

Friday, May 18, 2012

Wheat: opiate of the masses?


Last week I was aboard a cruise liner in the Caribbean. I had a lot of fun but was primarily there to participate in a kinda conference organised by low-carb advocate Jimmy Moore. I was privileged to share the stage with some very lovely and inspiration speakers, among them the US cardiologist Dr William (Bill) Davis. I was looking forward to meeting Bill because I’d had a skype conversation with him some months ago, and was impressed by his warmth, humour and humanity. In person, Bill did not disappoint, and he also gave what I thought was a fascinating presentation about the perils of one of the modern-day diet’s most ubiquitous components – wheat.

Bill is the author of the highly acclaimed and readable book Wheat Belly, which systemically makes a strong case for the elimination of this grain from our diets. His lecture on the low-carb cruise’ focused on this aspect of his work, and focused on what I took to be three key areas:

1. wheat’s content of the readily-digested starch amylopectin A, which is highly disruptive to blood sugar levels.

2. The lectin (toxin) in wheat known as ‘wheat germ agglutinin’ which can cause inflammation in the gut and elsewhere.

3. Gliadin – a component of gluten in wheat which has, among other things, drug-like effects.

It’s this last issue I’m going to focus on in this blog post.

In his lecture, Bill drew our attention to the fact that gliadin may not be fully digested in the gut, and give rise to small protein molecules known as ‘polypeptides’. These can sometimes penetrate the gut to gain access to the bloodstream, after which they also have capacity to make their way across the ‘blood-brain-barrier’. Once there, gliadin polypeptides can bind to opiate receptors in the brain. Opiates include chemicals like morphine, heroin and opium.

The body can generate chemicals which bind to opiate receptors which are termed ‘endorphins’. However, when a substance comes from outside the body, it is termed an ‘exorphin’. Gluten-derived exorphins can induce a feeling of mild euphoria. This might explain why tucking into bread, or a bowl of pasta, or some biscuits can seemingly be so intensely pleasurable for some. It might also explain why some struggle with leaving wheat alone.

One of the main reasons Bill highlighted the opiate effects of gluten is because it appears, to all intents and purposes, to be an appetite stimulate. Of course you’d expect anything that is somewhat addictive to drive us to consume more of it. And as Bill pointed out, there does seem to be some scientific evidence for this.

To understand the nature of this research, we need to understand the effects of the drug naloxone. This drug binds to opiate receptors, knocking off anything else that may be bound there. As a result, naloxone reverses the effects of opiate drugs like heroin and morphine, and quickly too.
So, what happens when normal wheat-consuming people are treated with naloxone? In one study, individuals were given access to a free food and their intakes measured over two meals approximately 5 hours apart [1]. On another occasion the experiment was repeated after naloxone had been administered to the study subjects. On this occasion, they consumed about 400 calories less.

In another study, ‘binge-eaters’ were given access to a free buffet with and without nalaoxone [2]. With naloxone on board, individuals ate 28 per cent less in the way of wheat-based foods such as crackers, pretzels and bread sticks.

My experience in practice tells me that the ability of wheat (and other gluten-containing foods such as barley and rye) to have addictive qualities varies quite a lot between individuals. It does seem to be a real phenomenon, though, and there’s no doubt in my mind that eliminating or dramatically reducing wheat consumption usually leads to a significant improvement in wellbeing, energy levels, mental function (and usually weight loss) in the majority of people.

Starchy foods, especially ‘healthy wholegrains’ are often vigorously promoted to those looking to eat a nutritious diet. Wheat has a reputation as the staff of life. In reality, though, it’s often the stuff of nightmares.

References:
1. Cohen MR, et al. Naloxone reduces food intake in humans. Psychosom Med. 1985;47(2):132-8.
2. Drewnowski A, et al. Naloxone, an opiate blocker, reduces the consumption of sweet high-fat foods in obese and lean female binge eaters. Am J Clin Nutr. 1995;61(6):1206-12.
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Read the full article here.

Wednesday, March 7, 2012

Fish oil: The natural triglyceride form is better


Fish oil: The natural triglyceride form is better

If you have a choice, the triglyceride form of fish oil is preferable. The triglyceride form, i.e., 3 omega-3 fatty acids on a glycerol “backbone,” is the form found in the body of fish that protects them from cold temperatures (i.e., they remain liquid at low ambient temperatures).
Most fish oils on the market are the ethyl ester form. This means that the omega-3 fatty acids have been removed from the glycerol backbone; the fatty acids are then reacted with ethanol to form the ethyl ester.

If the form is not specified on your fish oil bottle, it is likely ethyl ester, since the triglyceride form is more costly to process and most manufacturers therefore boast about it. Also, prescription Lovaza–nearly 20 times more costly than the most expensive fish oil triglyceride liquid on a milligram for milligram basis–is the ethyl ester form. That’s not even factoring in reduced absorption of ethyl esters compared to triglyceride forms. Remember: FDA approval is not necessarily a stamp of superiority. It just means somebody had the money and ambition to pursue FDA approval. Period.
Taking any kind of fish oil, provided it is not overly oxidized (and thereby yields a smelly fish odor), is better than taking none at all. All fish oil will reduce triglycerides, accelerate clearance of postprandial (after-eating) lipoprotein byproducts of a meal (via activation of lipoprotein lipase), enhance endothelial responsiveness, reduce small LDL particles, and provide a physical stabilizing effect on atherosclerotic plaque.

But if you desire enhanced absorption and potentially lower dose to achieve equivalent RBC omega-3 levels, then triglyceride forms are better.

Here are cut-and-pasted abstracts of two of the studies comparing forms of fish oil.

Bioavailability of marine n-3 fatty acid formulations.

Dyerberg J, Madsen P, Moller JM et al.
Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark.

Abstract

The use of marine n-3 polyunsaturated fatty acids (n-3 PUFA) as supplements has prompted the development of concentrated formulations to overcome compliance problems. The present study compares three concentrated preparations – ethyl esters, free fatty acids and re-esterified triglycerides – with placebo oil in a double-blinded design, and with fish body oil and cod liver oil in single-blinded arms. Seventy-two volunteers were given approximately 3.3g of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 2 weeks. Increases in absolute amounts of EPA and DHA in fasting serum triglycerides, cholesterol esters and phospholipids were examined. Bioavailability of EPA+DHA from re-esterified triglycerides was superior (124%) compared with natural fish oil, whereas the bioavailability from ethyl esters was inferior (73%). Free fatty acid bioavailability (91%) did not differ significantly from natural triglycerides. The stereochemistry of fatty acid in acylglycerols did not influence the bioavailability of EPA and DHA.
(Full text of the Dyerberg et al study made available at the Nordic Naturals website here.)




Eur J Clin Nutr 2010 Nov 10.

Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters.

Neubronner J, Schuchardt JP, Kressel G et al.
Institute of Food Science and Human Nutrition, Leibniz Universität Hannover, Am Kleinen Felde 30, Hannover, Germany.

Abstract

There is a debate currently about whether different chemical forms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are absorbed in an identical way. The objective of this study was to investigate the response of the omega-3 index, the percentage of EPA+DHA in red blood cell membranes, to supplementation with two different omega-3 fatty acid (n-3 FA) formulations in humans. The study was conducted as a double-blinded placebo-controlled trial. A total of 150 volunteers was randomly assigned to one of the three groups: (1) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as reesterified triacylglycerides (rTAG group); (2) corn oil (placebo group) or (3) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as ethyl ester (EE group). Volunteers consumed four gelatine-coated soft capsules daily over a period of six months. The omega-3 index was determined at baseline (t(0)) after three months (t(3)) and at the end of the intervention period (t(6)). The omega-3 index increased significantly in both groups treated with n-3 FAs from baseline to t(3) and t(6) (P < 0.001). The omega-3 index increased to a greater extent in the rTAG group than in the EE group (t(3): 186 versus 161% (P < 0.001); t(6): 197 versus 171% (P < 0.01)). Conclusion: A six-month supplementation of identical doses of EPA+DHA led to a faster and higher increase in the omega-3 index when consumed as triacylglycerides than when consumed as ethyl esters.
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Read the full article here.

Sunday, October 9, 2011

Why small LDL particles are the #1 cause of heart disease in the US



Why small LDL particles are the #1 cause of heart disease in the US

Posted on by Dr. William Davis

Ask your doctor: What is the #1 cause of heart disease in the US?

Let’s put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol
Too much saturated fat
Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I’d tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

–Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

–In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here’s a 2006 review.

–Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to “cut fat and eat more healthy whole grains.” Conventional diet advice has therefore triggered an expllosion in small LDL particles.

–When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either “pattern B,” meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus “pattern A,” meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called “pattern A.”

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with “pattern B” small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat (“wheat belly”) to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet
 

About Dr. William Davis

Dr. Davis is Medical Director of the Track Your Plaque program and advocate of early heart disease prevention and reversal. He practices preventive cardiology in Milwaukee, Wisconsin.

Saturday, September 10, 2011

Getting a CT Heart Scan - Dr William R Davis

Wheat Belly author Dr. William Davis answering questions about getting a CT Heart Scan.


Dr. William Davis from http://www.trackyourplaque.com/blog appeared as a guest on Jimmy Moore's "The Livin' La Vida Low-Carb Show" podcast http://www.thelivinlowcarbshow.com/shownotes and answers questions about why he believes the calcium heart scan is an effective means for heart disease prevention, which CT Heart Scan is the correct one to get done and where to go to do it, and why it's a simple, safe and effective means for knowing where you stand.
http://www.youtube.com/user/livinlowcarbman

Wednesday, August 31, 2011

Wheat Belly

Tom Naughton just reviewed the book Wheat Belly by Dr. William R. Davis cardiologist. See that review here.

I just received my Kindle e-book copy and will read it soon.

I stopped consuming wheat products about two years ago at the recommendation of Dr Davis for the treatment of lipid disorders (it has a dramatic effect on small LDL) )and heart disease. Since I have a history of CAD that has resulted in 6 heart attacks I am of course interested in finally doing something to reduce the progression of plaque growth. The only advice I have received previous to this is to reduce my serum cholesterol i.e. take a statin and eat a low fat diet. But in the process of doing that I had my first four heart attacks. I treated that 'risk factor' (cholesterol) over the course of many years and while doing so had my first 4 heart attacks. Clearly it was not attacking the disease, only a non-significant risk factor in my case.

I am now following the Track Your Plaque regimen of measuring plaque using a heart scan, advanced lipid testing (VAP NMR, Berkley) , treating lipid disorders shown to be correctable in clinical trials and observations, following the TYP diet and monitoring blood glucose levels. I have only been on board fully with this approach since Feb 2011 so it is a work in progress.

I first began learning about this approach to actually treat the disease rather than a single risk factor back in 2006 or so but it took my skeptical self a while to become convinced. After all it was not exactly Main Stream Medicine. Was it quackery or something more. It took a couple more heart attacks and the realization that MSM had not served me well other than to patch the damage but not to treat the disease, to push me over the edge. I began blogging some of what I was finding in early 2007 to, if you will, document and share my findings, and keep track of what I think is Credible Evidence leading me to where I am now.

The Kindle version of Wheat Belly is only ten bucks. It is not the whole answer, but it does, I think, point to what is a significant piece of the puzzle.

Thanks Tom for the review.

Thursday, April 7, 2011

Statin drugs do indeed provide real advantage...

According to cardiologist William R. Davis of Track Your Plaque...

 "...there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception."