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Wednesday, April 24, 2013

Calcium Controversy 3 - The role of the traffic cop

As discussed in my previous blogpost, calcium supplements have a tendency to get deposited in the blood vessel walls and thereby predispose to cardiovascular disease.
Now comes a saviour molecule to negate those effects. Not a new discovery. Just an old one with a new role. Would you believe it!! A VITAMIN.
Vitamin K2.

Vit K has always been known to have blood clotting properties. What wasn't well known was that it has 3 subtypes:

  • Vitamin K1, or phylloquinone, is found naturally in plants, especially green vegetables; K1 goes directly to the liver and helps maintain healthy blood clotting.
  • Vitamin K2, also called menaquinone, is made by the bacteria that line the gastrointestinal tract; it is found in poultry and dairy products as well as animal based foods. K2 goes straight to blood vessel walls, bones, and tissues other than the liver.
  • Vitamin K3, or menadione, is a synthetic form.

Vitamin K1 exclusively participates in blood clotting. K2 on the other hand comes from a whole different set of food sources, and its biological role is to help move calcium into the proper areas in the body, such as bones and teeth. It also plays a role in removing calcium from areas where it shouldn't be, such as in arteries and soft tissues.

"K2 is really critical for keeping our bones strong and our arteries clear"

How does K2 do the job?

Vitamin K2 helps to activate vitamin K-dependent proteins responsible for healthy tissues. In bone, it activates osteocalcin, a protein required to bind calcium to the mineral matrix, thus strengthening the skeleton. In circulation, Vitamin K2 participates in carboxylation of Matrix Gla Protein (MGP), the most potent inhibitor of arterial calcification known, lowering the risk of vascular damage.


For treatment of osteoporosis, calcium supplements used to be prescribed. To enhance the absorption of these calciums, Vitamin D was supplemented. It is now a proven fact that calcium supplements can increase the incidence of cardiac events.
When we take vitamin D, our body creates more of these vitamin K2-dependent proteins, thereby increasing the demand for K2. If K2 is not supplemented, there is a definite possibility of Vit D toxicity and calcification of the arterial walls. Thus, if we opt for oral vitamin D, we need to also consume in our food or take supplemental vitamin K2.

Summarizing things. The Vitamin D acts as a gatekeeper, facilitating the entry of the traffic - read Calcium. Vitamin K2 is the traffic cop directing the traffic in the right direction.
Lots of traffic -- but no traffic cop -- means clogging, crowding and chaos everywhere!

In other words, without the help of vitamin K2, the calcium that our vitamin D so effectively lets in might be working AGAINST us-- by building up our coronary arteries rather than our bones.

Wednesday, April 17, 2013

Statins: The Diabetes dilemma

Continuing our trend of discussing the latest controversies of medical sciences, this one has the potential of overshadowing all the others.

Statins - Atorvastatin, Simvastatin, Rosuvastatin, to name a few, is a group of drugs which were primarily used to reduce the lipid levels. Over the course of time, many beneficial effects of this class of drugs were unearthed which has led to widespread and over the counter use of these tablets.

These beneficial/pleiotropic effects of statins include plaque stabilization, reduction of inflammation, reversal of endothelial dysfunction, and decreased thrombogenicity.

Numerous trials have shown a benefit for statin therapy both as primary patients who have never had heart disease and are taking statins to lower their risk (so-called primary prevention) and secondary prevention of cardiovascular disease (CVD) and mortality. Trials like the Collaborative Atorvastatin Diabetes Study (CARDS), proved beyond doubt that patients with type 2 diabetes and other risk factors for CVD should be treated with a statin, apparently disregarding their initial LDL cholesterol level.
Also, according to the New Canadian guidelines, all patients with Diabetes should start taking statins when they turn 40.

Diabetes Dilemma:

A number of large, clinical trials have now shown that use of statins can increase the risk of developing type-2 diabetes by about 9 percent.
Risk factors for Diabetes
This is fairly serious, especially if you are in the large group of patients who have not yet had a cardiovascular event, but just take statin drugs to lower your risks of heart disease.

Statins reduce the levels of Coenzyme Q10 which is needed for energy and other cellular functions. Also, they reduce the levels of a protein GLUT4 which leads to insulin resistance and onset of type 2 Diabetes mellitus. Supplementation of CoQ10 may possibly negate this effect.

Complications of Diabetes

In one study, diabetes mellitus was diagnosed in 27% more patients receiving a statin (rosuvastatin) compared with patients receiving placebo (an identical appearing pill that does not contain medication), but patients receiving the statin had a significant 54% lower risk of heart attack, 48% lower risk of stroke, and 20% lower risk of death.

Symptoms of Diabetes
There is a wealth of clinical data showing that patients with diabetes mellitus benefit greatly from statin therapy to prevent cardiac events. The current data do not support discontinuing statins if you have diabetes mellitus or if you are newly diagnosed with diabetes mellitus.


What should people who are taking statins do? If these are prescribed for someone who has already had heart disease or a stroke, the benefit is overriding — no changes are suggested. However, physicians need to monitor the sugars of these patients. But in the vast majority of people who take statins — those who have never had any heart disease — there should be a careful review of whether the statin is necessary, in light of the risk of diabetes and the relatively small benefit that can be derived. Maybe a dose reduction or use of a less potent statin should be considered on an individual basis.

Wednesday, April 10, 2013

Fasting and Diabetes: Hand of God?

Fasting during Ramadan, a holy month of Islam, is an obligatory duty for all healthy adult Muslims.

Ramadan is a lunar based month and depending on the region and season, the timings of the fast may vary from a few hours to more than 20 hrs.
Muslims who fast during Ramadan must abstain from eating, drinking, use of oral medications, and smoking from predawn to after sunset; however, there are no restrictions on food or fluid intake between sunset and dawn. Most people consume two meals per day during this month, one after sunset, referred to in Arabic as Iftar (breaking of the fast meal), and the other before dawn, referred to as Suhur (predawn).

The sick are exempt from fasting as it may pose a serious health hazard. Diabetics fall in this category because their chronic metabolic disorder may place them at high risk for various complications if the pattern and amount of their meal and fluid intake is markedly altered.


Fasting during Ramadan has been uniformly discouraged by the medical profession for patients with diabetes. Fasting works against the principles of diabetes management. The small, frequent meals advised in diabetics turn into 2 large meals during fasting. The fluid intake drastically drops. Gorging and compensatory eating is difficult to avoid during the non fasting period. The daily exercise routine has to stop since it is not humanly possible to continue it during the fast and equally difficult to pursue during the non fasting period due to lack of time. The doses of all medications need to be altered predisposing to various complications. In keeping with this, a large epidemiological study EPIDIAR conducted in 13 Islamic countries on 13,000 individuals with diabetes who fasted during Ramadan showed a high rate of acute complications.


Needless to say, decreased food intake predisposes to severe hypoglycemia during the fasting period. This is much more so in those patients whose sugars are tightly controlled.


Most likely due to excessive reduction in dosages of medications to prevent hypoglycemia. Increased sugars in turn increase the risk of micro as well as macro vascular complications.


Type I diabetics are more prone to this complication especially if their sugars are poorly controlled.


Markedly reduced fluid intake coupled with increased urine frequency in uncontrolled diabetics may result in dehydration and electrolyte imbalance. This could lead to thrombosis. A report from Saudi Arabia suggested an increased incidence of retinal vein occlusion in patients who fasted during Ramadan.

It may be re-emphasized here that fasting is a personal decision significantly based on religious sentiments.

Several studies have been published later on the effects of fasting; some of the results are controversial. Most of them conclude that Ramadan fasting leads to significant body weight reduction and improvement of glycaemic control in diabetic patients with out other significant metabolic changes in lipids, uric acid and renal functions.

Despite the potential health risks of fasting in diabetics, the majority of studies have not shown significantly high rates of complications. On the contrary, there has been an improvement in the sugar levels during periods of fast. The underestimation of the incidence of hypoglycemia is however due to the fact that very few patients have a tight control of their glucose levels during the pre Ramadan period. But how do we explain the low incidence of the other known complications? We may have to accept the involvement of a Heavenly Hand in the protection against these untoward events.

I would like to conclude on a scientific note that the bulk of literature indicates that fasting in Ramadan is safe for the majority of diabetics patients with proper education and diabetic management. The patients on their parts need to be conscious of their disease and be compliant with their diet and drug intakes.

Monday, April 08, 2013

Bald is beautiful??

With more men choosing to shave their heads these days, it's clear that 'bald is beautiful'. However, is it really so beautiful?

Male pattern baldness evolution
Male pattern baldness, the commonest cause of baldness, has been linked to age, genetics, sex hormones (testosterone) and high levels of a protein called prostaglandin D2 on the scalp.

The role of testosterone in premature balding has led to the myth that going bald is a sign of virility. However, men with male pattern baldness aren't any more well-endowed with testosterone than other guys. Their hair follicles are simply more sensitive to the hormones.

Frontal baldness
However, male-pattern baldness is linked to an increased risk of coronary heart disease, but only if the baldness is on the crown of the head (vertex) instead of the front, according to a data analysis.
Findings indicated that the severity of baldness affected the risk of coronary heart disease. Men with both frontal and crown-top baldness were 69% more likely to have coronary artery disease than those with a full head of hair, while those with only crown-top baldness were 52% more likely and those with only frontal baldness were 22% more likely.
Vertex baldness

Explanations for the reasons behind the association vary, but include the possibility that baldness may indicate insulin resistance, a precursor to diabetes; a state of chronic inflammation; or increased sensitivity to testosterone. Each of those factors is involved directly or indirectly in promoting cardiovascular disease.

Although these findings are interesting, much more research is needed to confirm any link between male pattern baldness and an increased risk of coronary heart disease. In the meantime, it's more important to pay attention to your waistline than your hairline.

Friday, April 05, 2013

Drug Patents - The battle between generic and branded

Generic drugs are cheaper copies of brand-name drugs that have exactly the same dosage, intended use, effects, side effects, route of administration, risks, safety, and strength as the original drug. In other words, their pharmacological effects are exactly the same as those of their brand-name counterparts. For e.g. Metformin and Metoprolol are the generic versions of Glucophage and Lopressor respectively.

The generic vs brand name issue has been a hot topic in the Indian medical community ever since
Mr. Amir Khan raised this sensitive issue in his "Satyameva Jayate".

Big pharmaceutical companies spend hundreds of millions of dollars to bring a new drug brand to market. They protect that drug brand with a Patent that prevents anyone else from selling the active ingredient for a certain period of time. Eventually that patent expires — allowing another company to make another pill, a generic, with the same active ingredient. That's when the game changes.

Generic drugs can be legally produced for drugs where: 1) the patent has expired, 2) in countries where a patent(s) is/are not in force.

The expiration of a patent removes the monopoly of the patent holder on drug sales licensing.
Patent lifetime differs from country to country, and typically there is no way to renew a patent after it expires.

So, to counter this, the big Pharma players have devised new strategies.

Companies can get a fresh patent for an already patented drug by altering its formula or changing its dosage. The companies contend that even minor improvements in medicines — changing a pill dosage to once a day instead of twice a day — can have a significant impact on patient wellness. But critics say a majority of drug patents given in the United States are for tiny changes that often provide patients few meaningful benefits but allow drug companies to continue charging high prices for years beyond the original patent life.

They point to AstraZeneca, for example, which extended for years its franchise around the huge-selling heartburn pill Prilosec by slightly altering the chemical structure and renaming the medicine Nexium.

Passed under international pressure, India’s 2005 patent law for the first time allowed for patents on medicines, but only for drugs discovered after 1995.

The controversy now begins.

Many people become concerned because generic drugs are often substantially cheaper than the brand-name versions. They wonder if the quality and effectiveness have been compromised to make the less expensive products. The FDA (U.S. Food and Drug Administration) requires that generic drugs be as safe and effective as brand-name drugs.

Actually, generic drugs are cheaper only because the manufacturers have not had the expenses of developing and marketing a new drug.

Generic and brand-name drugs are supposed to be “bioequivalent” — in other words, they’re supposed to get the same key substance into the human body at roughly the same blood concentration level. But, the “Most regulatory bodies require bioequivalence parameters to fall within a 25% window, meaning that one generic version could conceivably have 80% bioequivalence to the reference product, whereas another could have 125% bioequivalence.” Thus, in some cases, the generic might not have the same effect as the brand-name drug.

When multiple companies begin producing and selling a drug, the competition among them can drive the price down even further.
Thus, the generic versions significantly bring down the cost of therapy which is a real boon to patients in the developing countries where the health insurance infrastructure is practically nonexistent.

However, this significant reduction in cost of drugs can drastically cut the profits of the branded ones which could prove a deterrent to future research and analysis.

The debate over global drug pricing is one of the most contentious issues between developed countries and the developing world. While poorer nations maintain they have a moral obligation to make cheaper, generic drugs available to their populations — by limiting patents in some cases — the brand name pharmaceutical companies contend the profits they reap are essential to their ability to develop and manufacture innovative medicine.

Pls read the sequel on