Egg Consumption doubles Cardiometabolic Risk

The gut flora or microbiota is undoubtedly crucial to the digestive process. However, there is growing interest in the role of the gut microbiota as an environmental factor influencing propensity for cardiometabolic disease. Studies have implicated the gut microbiota in susceptibility to obesity and insulin resistance; germ-free mice fed a high-fat, high-carbohydrate Western-style diet were protected against diet-induced obesity, glucose intolerance and insulin resistance.

More recently, research has linked dietary lipid intake, the gut microbiota and increased risk for atherosclerosis.(2,3) Cholesterol-rich foods, such as egg yolks, contain phosphatidylcholine which is hydrolysed by phospholipase enzymes to release choline. The gut microbiota then convert choline to trimethylamine (TMA), whichundergoes oxidation in the liver to trimethylamine N-oxide (TMAO), released into the plasma.

In mice susceptible to atherosclerosis fed a diet supplemented with phosphatidyl choline, there was an increase in plasma levels of TMAO concomitant with increased atherosclerotic plaque development. Mechanistically, increased dietary choline was associated with suppression of multiple macrophage scavenger receptors which protect against atherosclerosis.3 These data therefore implicate excess dietary choline as an emerging modifiable risk factor for cardiovascular disease, mediated by the gut microbiota.

These findings may be relevant in the light with recent research which showed an association between egg yolk consumption and carotid plaque burden. Individuals consuming 3 or more eggs per week had a significantly higher plaque burden that those with reduced consumption. This suggests that egg yolk consumption should be reduced or avoided in high-risk individuals with established cardiovascular disease. Consumption of a large egg (which equates to about 200 mg of dietary cholesterol) not only increases the susceptibility of low-density lipoproteins (LDL) to oxidation, but also increases postprandial lipaemia, and potentiates the adverse effects of dietary saturated fat. Additionally, egg consumption effectively halves postprandial clearance of atherogenic chylomicron remnants, which implies a need to re-consider egg yolk consumption in individuals with cardiometabolic disease, including those with diabetes. Indeed, in observational studies, regular egg consumption was associated with increased risk of new-onset diabetes, cardiovascular disease and all-cause mortality. These epidemiological data, together with the FOCUS paper, provide a strong rationale for a prospective randomized trial comparing the effects of consumption of eggs or egg white-based substitutes on hard clinical outcomes.  Currently, international guidelines are inconsistent in considering the dietary cholesterol. Currently, international guidelines are inconsistent in their consideration of dietary cholesterol. There are also misconceptions that because of the efficacy of statins in lowering plasma total cholesterol and LDL cholesterol, consideration of dietary cholesterol is less relevant in statin-treated patients. Yet even with intensive statin therapy, there remains about 70% residual cardiovascular risk.

by

Dr.Akshaya Srikanth, Pharm.D

Pharm.D in India: What is known and What is unknown ?

Doctor of Pharmacy (Pharm.D) in India has created a huge hike on young pharmacists, expecting the future is much better than the other branches of pharmacy. Pharm.D's syllabus is we framed with lot of debates and observations from the developed world to provide a competent clinical pharmacist for the better health care in India. See the syllabus the other health care professionals were excited to see the practicality of this course in their work place. But, theoretically Pharm.D has made a huge impact on the developed nations and developing nations to adopt the India Pharm.D syllabus a standard one to practice in their own countries. To the same, the Indian Pharm.D has many pitfalls in practicality, which is hard to answer the route cause. For instance, a competent clinical pharmacist needed more practical training which need much focus on patient care by training them in the wards and engaging them in all the activities that can make them to learn how to implement the clinical pharmacy and collaborative work with other health professionals. Due to lack of competitive faculties the scope of bed-side teaching was negligible. Its fact, when Pharm.D students enter into the wards, they see the nursing staff training their nurses, Doctors training their medicos but Pharm.D students were relaying on the medical doctors to provide some support as the faculties never likely to participate in the bed-side teaching and working with the health professionals in the wards.

Increasing number of colleges increased the demand of Pharm.D admission, but there is none to answer the practicality of their roles and jobs. Disparities in training and unsuccessful competencies with poor health care acceptance kept the Pharm.D's into dilemma. Furthermore, it also made a lot of confusion among the student minds and unable to fulfill their dreams. For instance, course such as  Pharmacoepidemiology and clinical research were elaborative in syllabus, but faculties unable to engage them in any activities such visiting clinical research sites, engaging them in some pharmacovigilance activities. Furthermore, the organizations well focusing on conferences for showoff and unnecessary hikes over the Pharm.D without know the practical barriers faced by the students. For instance, there are many pharmacy organizations inviting the international delegates to participate in the national and international conferences, but unable to engage the Indian Pharm.D's to get trained in overseas.

Now the number of Pharm.D's increasing and coming out with any vision. This is because of lack of planning and support from the Pharmacy board. This situation is especially burning in southern states where the number of colleges are more than that of other parts of India. All colleges promising to give admission but unable to secure them in jobs. The student associations such as "IPSF", and "IPA-SF" etc., are focusing on conferences and international fame rather to supporting the local Pharm.D students. The silence answers from the pharmacy leaders increasing the tensions in the student mind. There is much more needed to work at ground level, focusing on providing standard practical training rather basic theoretical knowledge, providing a scope and hope on the Pharm.D's for securing the jobs is crucial.

In conclusion, Pharm.D's are currently in great frustration and needed support from all phases for the future of clinical pharmacy in India. Further, clinical pharmacy is a practice of patient care through pharmaceutical care. If the theoretical knowledge can fulfill the dream then we are in world of delusion.
by
Dr.Akshaya Srikanth, Pharm.D
Pharm.D India

Feed your Brain with ECG Today

Many people think electrocardiograph (thusly called ECG or EKG) a tough talk to understand and interpret. This is not such a huge task or need to do specialization in cardiology. This is just cardiology, simple biological pipes and wires. ECGs are simpler still, being a moving real time map of the “wires” part and how they conduct electricity.  Reading EKGs only seems hard because most cardiologists use long (expensive) words.

Most healthy hearts pump blood through the body when stimulated by an electrical signal that travels along predetermined pathways.This causes the cardiac cells to contract in just the right order, resulting in a magical four chambered pumping action. 

An EKG is a graph tracing the strength and direction of this electrical signal. Leads equipped with conductive goo are placed on different parts of the body allowing a view of the heart from different angles. If the electrical activity of the heart at any given moment is traveling toward the lead being viewed, the line on the graph goes up (positive deflection).  If the electrical activity is traveling away from the lead, the line goes down (negative deflection). This graph is being traced by a stylus on a moving piece of graph paper. In a normal healthy heart, an ECG representing one complete heartbeat looks about like this :

That first petite little hump, affectionately called the P wave, represents the electrical signal that starts in a group of cells called the Sinoatrial Node. This signal then travels through the atria (the smaller and upper two chambers of the heart) causing them to contract and push blood in to the larger and more powerful ventricles below.

The “PR Interval” segment represents a delay in the signal at another grouping of cells called the AtrioVentricular Node.This delay allows time for the atria to completely deliver their bounty into the Ventricles. With perfect timing this signal continues through the Bundle of His.The signal splits and speeds along down the left and right bundle branches, making its way to the Purkinje fibers and turning north again.This stimulates those Ventricular beefcakes to contract and deliver their payload to the lungs and body (if hearts had biceps, the left ventricle would be the proverbial “gun show”….it’s such a glory hog!).

The journey causing this second contraction through the ventricles is represented by the QRS portion of the ECG. The larger T wave which then finishes off our heartbeat is the repolarization of the ventricles.I know what you’re thinking, either “what in the what now goes where?” or hopefully, “what wave represents the repolarization of the atria”? Well, the repolarization of the atria is buried in the larger signal of the QRS and therefore not visible on the graph.

This pattern is called normal sinus rhythm.  It is the basic ECG of any normal healthy heart. Naturally, there are variations of normal within the healthy population. For example, my boyfriend is very fit and has a *huge* R wave (hands off his big left ventricle ladies, it’s all mine! And don’t get me started on his early repolarization…and no…being early in this case is definitely not a bad thing). However, anything outside of the normal range is analyzed along with the patient’s symptoms to create a working diagnosis.There are several types of common abnormalities. A PR interval that is too long is called a first degree block. A QRS that takes longer than .12 seconds is likely to be caused by a delay in one or both bundle branches, called a bundle branch block. A complete lack of P waves, and in their place a squiggly line, combined with an irregular heartbeat is likely to be atrial fibrillation. What really gets a Paramedic or ER doctor excited is when they see an elevation of the ST segment in a few consecutive leads.This is referred to as an ST elevation myocardial infarction (heart attack) and generally results in a speedy trip to the catheterization. 

Feeding points:

1) Each small box on the modern ECG strip represents 0.04 seconds on the horizontal axis.

2) ECG paper is calibrated to move at 25mm per second past the stylus.

3) The ECG was invented by the Dutch Dr. Willhelm Einthoven in 1903, for which he received the Nobel Prize in 1924. More impressively, he also had a triangle named after him.

4) It is very rare, but possible for an ECG to show a flat line, called asystole, when in fact the heart is still beating and producing a pulse.  It is because of this that it’s common practice to confirm death in a patient by looking for asystole in more than one lead.

5) Conversely it is also possible, and more common, to have an ECG show heart activity, and even normal sinus rhythm, after a person has died and their heart is no longer pumping blood. This is called a PEA, pulseless electrical activity, and shows what is left of the heart’s intact electrical system after the muscle itself has failed.

I hope you understand well. 

Thanking you

Dr.Akshaya Srikanth B, PharmD

Cardiac Biomarkers

A blood screening technology has uncovered many biomarkers that improve the prediction of the risk for heart attack or stroke with in the next 15 years. The blood profiling technique may eventually help doctors to identify those people who would benefit the most from early treatment and high-throughput profiling of circulating metabolites may improve cardiovascular risk prediction over established rik prediction over established risk factors. 

Biomarkers can potentially be used to detect and monitor a wide range of cardiac conditions in the critical care setting. Currently the only biomarker acceptable for changing management in acute coronary syndrome is the troponin test. In the future, a tailored multi-marker approach may have use in guiding diagnosis and therapy – this is a long way off!

POTENTIAL USES OF CARDIAC BIOMARKERS

Myocardial Ischemia

·         Troponin

·         H-FABP

·         ischaemic modified albumin

Thrombosis

·         CRP

·         ESR

·         different binding proteins

·         Myocardial injury

·         Troponin (level peaks at 12h, proportional to infarct size, but altered by washout phenomenom after reperfusion therapy)

·         CK

·         CK-MB

·         myoglobin

·         AST

·         LDH

Novel: copeptin (C-terminal provasopressin), BNP/ NTproBNP, GP-BB, myleoperoxidase, pregnancy associated plasma protein A

Inflammation, endothelial activation and neutrophilic activation

·         CRP

·         ESR

·         PaPPA

·         endothelin/ CTproET-1

·         adrenomedullin/ MRproADM

·         myeloperoxidase

·         matrix metalloproteinases (MMP9, MMP2, TIMP1)

Heart failure

·         BNP/ NTproBNP

·         ANP/ N-ANP/ MRproANP

·         Troponin

·         IL18

·         CA125

·         Urocortin

Sepsis-induced myocardial dysfunction

·         Troponin

·         BNP/ NTproBNP

·         Right ventricular strain in pulmonary embolism

·         Troponin

·         BNP/ NTproBNP

ADVANTAGES AND DISADVANTAGES 

In addition these biomarkers mentioned above four new biomarkers were identified in 2015. The scientists identified over 200 biomarkers for body metabolism from a single blood sample using Nuclear Magnetic Resonance (NMR) spectroscopy. The perspectives of new biomarkers for future cardiovascular disease were Phenylalanine, a common amino acid, and the amount of monounsaturated fat in the blood; higher concentrations were linked with higher disease risk. These two biomarkers were as strong predictors of future heart disease as the measures bad cholesterol or blood pressure. In addition, higher blood levels of both omega-3 and omega-6 fatty acids were linked with lower risk for cardiovascular disease. All these molecules are normally present in everyone's blood, but it is the amount of these molecules that was shown to be reflecting the cardiovascular health. 

These new biomarkers can help to better assess the complex molecular processes behind the development of cardiovascular disease. The improved prediction of cardiovascular risk also suggests cost saving in healthcare by advanced biomarker profiling. The low-cost blood screening technology opens a treasure trove to understand the molecular mechanism of heart disease and other metabolic disease.

by 

Dr.Akshaya Srikanth Bhagavathula, Pharm.D 

for Pharm.D India

Trigeminal Neuralgia: The suicide disease

Trigeminal Neuralgia is a type of facial pain / headache causing sharp, shooting pain on one side of the face. It is one of the most painful diseases known to mankind. It is also called ‘suicide disease’, because of the severity of the pain.

Symptoms

People suffering from trigeminal neuralgia usually have a sharp, shooting, electric shock like pain on one side of the face / head. Trigeminal nerves are basically a set of 3 nerves that provide sensation to either side of the face. Trigeminal pain can affect different parts of the face. Initially the sharp pain is occasional and very short lasting. Gradually the pain becomes more permanent. It is more common in elderly people, over the age of 50 years. It is slightly more common in women.

Triggers Trigeminal Pain Attacks

Trigeminal neuralgia pain can be triggered by trivial things like cold air, touch, speaking, shaving, brushing teeth and chewing food. Pain is usually felt in the cheeks, lips, nose, ears, eyes, teeth, jaw, scalp or the entire side of the face. It almost always affects only one side of the face. Unlike migraine headache, the trigeminal pain does not change from one side of the face to the other. It is very common to find trigeminal neuralgia sufferers refusing to talk /open their mouth. They may cover that part of the face to avoid touch or air contact. Frequently they end up with dentists, thinking it is a dental problem.

How is trigeminal neuralgia diagnosed?

If trigeminal neuralgia is suspected, it is advisable to consult with a neuro physician or pain physician. After having the clinical history and performing a neurological examination, the physician may order a MRI or CT of the brain. Once diagnosis is confirmed, appropriate treatment is started.

How is trigeminal neuralgia treated?

Initial treatment for trigeminal neuralgia includes medications like carbamazepine (tegretol), oxcarbazepine, gabapentin, pregabalin, baclofen, etc. Typically, the medication is started at low doses and adjusted according the effect. With medications, mild cases of trigeminal neuralgia pain can be controlled. Taking long term medications can cause some side effects.

What are the advanced treatment options for trigeminal neuralgia?

If oral medications are not providing adequate satisfactory pain relief or if there are medication related side effects, other advanced options are available. Radiofrequency ablation of the trigeminal ganglion is newer modality of treatment available for trigeminal neuralgia sufferers. Radiofrequency thermal ablation of trigeminal ganglion, performed under x-ray guidance, provides safe, long term relief from trigeminal neuralgia pain.

It is a day care procedure performed under IV sedation. Once RF ablation is performed, patient can stop taking usual oral medications. Percutaneous pain interventional procedures like radiofrequency ablation of trigeminal ganglion are repeatable at a later date, if required. Trigeminal pain sufferers above 50 years of age are also good candidates for radiofrequency ablations. Older techniques like glycerol injections and balloon compression have been replaced by RF ablations now. Majority of insurance companies including the government schemes approve RF ablation for trigeminal neuralgia sufferers.

What is the role for surgery in trigeminal neuralgia?

Surgeries are reserved for patients, not responding to oral medications and conservative management. It may be suitable for trigeminal neuralgia due to secondary causes like tumours or trigeminal neuralgia in younger patients.Surgeries called microvascular decompression are offered by neurosurgeons for trigeminal neuralgia. Microvascular decompression surgeries have more risk involved and are costly. If performed successfully, these neuro surgeries can provide long term pain relief. Thanks to the advent of all the above mentioned treatments, trigeminal neuralgia sufferers don’t have to suffer in pain anymore.

by

Dr.Akshaya Srikanth B

LIPIDS AND STROKE: A RESEARCH UPDATE

Stroke, predominantly ischaemic stroke, is a leading cause of mortality, morbidity and  long-term disability. Moreover, the fact that one in four strokes occur in individuals who have previously had a stroke, highlights the need for urgent action to reduce the residual risk of recurrent events.

Guidelines recommend low-density lipoprotein cholesterol (LDL-C) as the primary lipid target for reducing the risk of recurrent stroke. However, mounting evidence suggests that other lipid parameters might be also predictive of cardiovascular risk and provide additional benefit. Little is so far known about the effects of non-traditional lipid factors or emerging biomarkers on recurrent stroke risk.

Previous studies have indicated that atherogenic dyslipidaemia, the combination of elevated triglycerides and low plasma concentration of high-density lipoprotein cholesterol (HDL-C) may be implicated in recurrent stroke risk. For example, in the Vitamin Intervention for Stroke Prevention study database including 3680 patients with a recent 120 days noncardioembolic stroke, the triglycerides/high-density lipoprotein cholesterol (HDL-C) ration, often termed as the atherogenic index, was consistently and independently associated with stroke risk, with the highest triglycerides/HDL-C ratio quintile associated with a 56% increase in recurrent stroke risk versus reference (low quintile). Consistent findings were also reported for the Women's Health Initiative Observational Study in Postmenopausal women. 

Recent analyses from the PERFORM (Prevention of Cerebrovascular and Cardiovascular Events of Ischemic Origin With Terutroban in Patients With a History of Ischemic Stroke or Transient Ischemic Attack) and SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) trials, discussed in this month’s Landmark trial, add to this body of evidence. Atherogenic dyslipidaemia, defined as low HDL-C (?40 mg/dL or 1.01 mmol/L) and elevated triglycerides (?150 mg/dL or 1.7 mmol/L), was an important contributor to residual cardiovascular risk in patients with a prior stroke or transient ischaemic attack (TIA) who were receiving best medical therapy, including statin. In both trials, patients with this dyslipidaemic profile had a 36-40% increased risk of recurrent stroke, despite other cardiovascular risk factors including LDL-C being well controlled by best evidence-based medicine.

The question remains: how best to address this high residual risk for recurrent stroke. Clinical trials of current therapies, including fibrates and niacin, have been less than definitive. Whether novel therapies offer future potential has yet to be addressed by prospective trials specifically targeting atherogenic dyslipidaemia. Indeed, the Residual Risk Reduction Initiative echoes the call to action made by the authors of this analysis for trials in this patient population. 

Finally, while much of the focus has been on lipid-related residual cardiovascular risk, a recent analysis from the Treating to New Targets Study also makes the case for consideration of non-lipid biomarkers. In patients with established coronary heart disease (CHD) at LDL-C goal, plasma levels of lipoprotein(a), neopterin, NT-proBNP, and sRAGE were all shown to be associated with the risk of recurrent major cardiovascular events. Lipoprotein(a) has already been linked with risk for ischaemic stroke, however, with the exception of niacin, current therapies are ineffective in targeting this lipoprotein. Whether novel agents in development may provide benefit has been the subject of much interest, given that monoclonal antibody therapy targeting PCSK9 has been shown to be effective in lowering liporprotein(a) levels by 25-30%, on top of statin therapy. Clinical trials in patients with a previous stroke are clearly needed to address the paucity of evidence relating to emerging biomarkers that may contribute to residual risk for recurrent stroke in patients receiving best evidence-based medicine. 

by

Dr.Akshaya Srikanth, PharmD.

2 of 3 Smokers Will Die Early If They Don’t Quit

Two-thirds of smokers will die early from their habit if they don’t quit, a new study suggests.

The findings indicate that it’s never too late to quit smoking, one expert said.

Researchers analyzed data from more than 200,000 people taking part in a study conducted by the Sax Institute in Australia. The study is a long-term investigation of healthy aging.

“We knew smoking was bad, but we now have direct independent evidence that confirms the disturbing findings that have been emerging internationally,” Emily Banks, scientific director of the Sax study and a researcher at the Australian National University, said in an institute news release.

“Even with the very low rates of smoking that we have in Australia, we found that smokers have around threefold the risk of premature death of those who have never smoked. We also found smokers will die an estimated 10 years earlier than nonsmokers,” she added.

Compared with not smoking, having just 10 cigarettes a day doubles the risk of dying early. And smoking a pack a day increases the risk four- to fivefold, according to the study published Feb. 24 in the journal BMC Medicine.

It was long thought that smoking-related diseases would kill about half of smokers early, but newer research has put the figure as high as 67 percent. 

My Suggestion: “It’s never too late to quit, no matter what your age or how much you smoke,”

by Dr.Akshaya Srikanth B, Pharm.D, BCPS.

Cola Raises Cancer Risk Due to Its Caramel Coloring

Research has found that 4-methylimidazole (4-Mel), the chemical that gives cola its

appealing caramel color is a potential carcinogen.

There aren't any federal regulations that restrict use of 4-Mel, but according to the report, more than half of Americans between age 6 to 64 drink enough soda on a regular basis to elevate their cancer risk.

Researchers from the Consumer Reports and the Center for a Livable Future at Johns Hopkins Bloomberg School of Public Health, tested 110 samples of cola and other soft drink beverages.

All of the samples, except for the clear beverages, contained 3.4 to 352.5 micrograms of 4-Mel per 12-ounce bottle or can. While there aren't federal regulations on how much of the chemical manufacturers can put in beverages, California does require companies to include a cancer warning label if the drink contains more than 29 micrograms in a 12-ounce bottle or can. The average person age 6 to 64 drank as much as two and a half cans of cola per day. Approximately one-third of children between ages 3 and 5 drank two-thirds of a can each day. People between age 16 and 44 were the most frequent cola drinkers, consuming as many as three cans per day.

Through this analysis, the researchers concluded that within the next 70 years, there could be at as many as 5,000 incidences of cancer directly related to cola consumption. But cracking down on the soft drink industry won't completely eliminate the chemical from the American diet. Unfortunately, dark-colored carbonated beverages are not the only source of 4-Mel. 

The chemical is also used in soy and barbecue sauce, pancake syrup and some soups. The study is published in PLOS One.

Read more: Cola Raises Cancer Risk Due to Its Caramel Coloring
by 
Dr.Akshaya Srikanth Bhagavathula, PharmD. BCPS.