Certain vaccines are actually recommended during pregnancy: the Tdap vaccine (tetanus, diphtheria, and pertussis), which helps protect against whooping cough, as well as the flu shot.
You can get the flu shot during any trimester or before pregnancy, depending on whether it’s flu season when you’re expecting. Experts generally recommend that pregnant women get the Tdap between the 27- and 36-week marks. Any friends and family members who will spend time around your newborn should get these vaccines, too.
Then there are the vaccines you definitely should not get if you’re pregnant. Types made with live strains of a virus could potentially transmit the virus to the baby.
The MMR (measles, mumps, and rubella) vaccine is a live-virus vaccine; women are advised to wait at least a month after receiving it before getting pregnant. Same goes for the varicella vaccine (for chicken pox). Many women received these vaccines as children, but your doctor will want to make sure you’re immune by doing a pre-pregnancy blood test.
Rubella, for example, can cause serious birth defects if a pregnant woman gets infected—so it’s important to make sure you’re up-to-date on all vaccinations before you try to conceive.
00seshunarayanahttps://imedworks.com/wp-content/uploads/2020/09/MedWorks-Logo-02-300x300.pngseshunarayana2020-08-10 20:53:502020-08-10 20:53:50Is it safe to get vaccines when you’re pregnant ?
If what some scientists are saying is true, preventing both heart disease and diabetes could be as simple as popping a single pill. Soon, preventing both heart disease and diabetes could be as simple as popping a single pill, if predictions by a team of scientists prove true.
A large analysis of genetic data found that both the conditions, which are the leading causes of death and illness across the world, are linked by the same genes. The team led by researchers in the Perelman School of Medicine at the University of Pennsylvania first looked into what causes Type 2 diabetes (T2D) and then clarified how T2D and coronary heart disease (CHD) are linked.
Examining genome sequence information for more than 250,000 people, the researchers first uncovered 16 new diabetes genetic risk factors and one new CHD genetic risk factor; hence providing novel insights about the mechanisms of the two diseases.
They then showed that most of the sites on the genome known to be associated with higher diabetes risk are also associated with higher CHD risk. For eight of these sites, the researchers were able to identify a specific gene variant that influences risk for both diseases. The shared genetic risk factors affect biological pathways including immunity, cell proliferation, and heart development.
The findings add to the basic scientific understanding of both these major diseases and point to potential targets for future drugs. “Identifying these gene variants linked to both type 2 diabetes and CHD risk in principle opens up opportunities to lower the risk of both outcomes with a single drug,” said co-senior author Danish Saleheen. “From a drug development perspective, it would make sense to focus on those pathways that are most strongly linked to both diseases,” Saleheen said.
The researchers found evidence that, on the whole, the genetic link between the diseases appears to work in one direction, so that risk genes for type 2 diabetes are much more likely to be associated with higher CHD risk than the other way around. Additionally, there could be some pathways where pharmacological lowering of one disease increases the risk of the other.
The scientists also found that diabetes-linked gene variants tend to differ in their apparent effects on CHD risk, depending on their mechanisms. Variants that increase the chance of obesity or high blood pressure, for example, appear to boost CHD risk more strongly than variants that alter insulin or glucose levels. The dual-effect risk loci also include the region covering the gene FABP4, which is already being investigated for its potential as a diabetes and heart-disease drug target. In mouse studies, inhibition of this gene’s protein has been shown to have anti-atherosclerotic, i.e., helps fight thickening and hardening with fat on the inside of arteries and anti-diabetic effects.
Saleheen, co-senior author Benjamin F. Voight and their colleagues now plan further investigations of the dual-risk genes uncovered in the study. The researchers also hope to learn more about the biology of the newly discovered dual-risk genes by studying people who have mutations in those genes, Saleheen said. The study is published in Nature Genetics.
Researchers have found that a naturally occurring protein helps to protect the retina against glaucoma.
Scientists may be on the brink of a new strategy to prevent blindness, after discovering a naturally occurring protein that protects the eye from one of the leading causes: glaucoma. Glaucoma is an umbrella term for a number of diseases that damage the optic nerve, which is the cluster of nerve fibers that links the retina – the light-sensitive tissue that lines the back of the eye – to the brain.
Optic nerve damage disrupts the transmission of visual signals to the brain, which can result in vision loss and blindness.
Glaucoma is most commonly caused by a buildup of eye pressure, which can damage the optic nerve. However, the precise mechanisms by which optic nerve damage occurs have been unclear, but researchers from Macquarie University in Australia may have shed some light.
The team found that a protein called neuroserpin plays a key role in retinal health, but that this protein is inactivated in glaucoma. They suggest that their findings may lead to much-needed strategies to prevent and treat the disease.
Lead study author Dr. Vivek Gupta, of the Faculty of Medicine and Health Sciences at Macquarie University, and colleagues recently published their results in the journal Scientific Reports.
Neuroserpin and glaucoma
Neuroserpin is already established as a protein that blocks the activity of an enzyme called plasmin, protecting neurons, or nerve cells, against plasmin-induced damage.
For their study, Dr. Gupta and colleagues set out to determine how neuroserpin and plasmin are affected by glaucoma.
The researchers came to their findings by analyzing retinal cells derived from humans with and without glaucoma, as well as retinas from rat models of the disease.
The analysis revealed that neuroserpin is deactivated in response to oxidative stress, which can be triggered by environmental factors such as air pollution.
Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) – which are molecules that can damage cell structures – and the body’s ability to offset their harmful effects.
Interestingly, the researchers found that neuroserpin was inactive in retinal cells from glaucoma patients and in the retinas of glaucoma rat models, which prevented the protein from inhibiting plasmin activity.
“Over a long period of time,” explains Dr. Gupta, “increased enzyme activity gradually digests the eye tissue and promotes cell death causing the adverse effects associated with glaucoma.”
‘Breakthrough findings’
It is estimated that glaucoma affects around 2.2 million adults aged 40 and older in the United States, and it is one of the country’s leading causes of vision loss and blindness.
There is currently no cure for glaucoma, but there are treatments that can help to slow progression of the disease if it is detected early enough.
Dr. Gupta and team hope that their findings will open the door to new strategies that could help to prevent or treat glaucoma.
“Ophthalmologists and vision scientists have always wondered what damages the optic nerve in the back of the eyes, which is widely observed in glaucoma,” notes study co-author Dr. Mehdi Mirzaei, of the Department of Chemistry and Biomolecular Sciences at Macquarie University.
“The breakthrough findings of this study,” he adds, “help us understand the disease mechanism and answer a key question that has eluded scientists for several years.”
“This long-term collaborative study has opened up a completely new line of investigation in glaucoma research that will lead to new treatment avenues for the disease.” Dr. Vivek Gupta In future studies, the team plans to investigate whether or not antioxidants – which are molecules that help to prevent cell damage caused by ROS – could be an effective treatment for glaucoma.
00seshunarayanahttps://imedworks.com/wp-content/uploads/2020/09/MedWorks-Logo-02-300x300.pngseshunarayana2020-08-10 18:52:512020-08-10 18:52:51Natural protein may help to prevent blindness
Scientists found that Hu-ink kills cancer cells in a laboratory dish. Under normal conditions, the ink is non-toxic. The deadly disease cancer often sneaks up on patients. While the cure for cancer is still being researched, scientists claim that a plant-based ink, that has been used by Chinese calligraphers for hundreds of years, could non-invasively kill cancer cells. As cancer cells leave a tumour, they frequently make their way to lymph nodes, which are part of the immune system. In this case, the main treatment option is surgery, but this can result in complications.
Photothermal therapy (PTT) is an emerging non-invasive treatment option in which nanomaterials are injected and accumulate in cancer cells. A laser heats up the nanomaterials, and this heat kills the cells. Many of these nanomaterials are expensive, difficult to make and toxic.
However, a traditional Chinese ink called Hu-Kaiwen (Hu- ink) has similar properties to the nanomaterials used in PTT. For example, they are the same colour, and are both carbon-based and stable in water. The researchers including those from Fudan University and Shanghai Jiao Tong University in China analysed Hu-ink and found that it consists of nanoparticles and thin layers of carbon. When Hu-ink was heated with a laser, its temperature rose by 55 degrees Celsius, much higher than current nanomaterials.
Under PPT conditions, the Hu-ink killed cancer cells in a laboratory dish, but under normal conditions, the ink was non-toxic. This was also the scenario observed in mice with tumours. The researchers also noted that Hu-ink could act as a probe to locate tumours and metastases because it absorbs near-infrared light, which goes through skin.
00seshunarayanahttps://imedworks.com/wp-content/uploads/2020/09/MedWorks-Logo-02-300x300.pngseshunarayana2020-08-10 18:31:202020-08-10 18:31:20Hope for cancer patients: Ancient Chinese ink could non-invasively treat the disease
In general, breast cancers could fall into 4 categories based on the presentation:
1. With no external signs but picked up on screening with mammography or ultrasound.They are non palpable,pre clinical.
2. This group present with symptoms mostly a lump in the breast mostly upper outer quadrant,but there is no hard and fast rule.
3. Group is called locally advanced where the swelling has gone beyond an operable stage(over 5 cms or with skin ulcers or tethering or massive lymph nodes ulcerating or not but with no features of dissemination)
4. These are the patients in whom the disease has spread to Liver,Lung,Brain ,Bones,Viscera or any other organs.Hence the signs and symptoms differ.
In general AJCC (American Joint Committee on Cancer) describes it in the following way. According to the American Cancer Society, any of the following unusual changes in the breast can be a symptom of breast cancer: – Swelling of all or part of the breast – Skin irritation or dimpling – Breast pain – Nipple pain or the nipple turning inward – Redness, scaliness, or thickening of the nipple or breast skin – A nipple discharge other than breast milk – A lump in the underarm area
These changes also can be signs of less serious conditions that are not cancerous, such as an infection or a cyst. It’s important to get any breast changes checked out promptly by a doctor. One should practice self examination.All those who are having menstruation should examine breasts during mid cycle and post menopausal women on any fixed day of the month regularly.
Do not ignore warning signs
Many a time it save lives. As a surgical oncologist and re constructive surgeon,and a specialist in breast diseases,and an ardent believer or breast preservation treatment protocols(Cosmetic oncology). I feel over 99% of the times breast preservation is possible without jeopardising oncological benefits,in those whom early detection is done. Please remember,breast cancer is a younger lady’s problem.
Share this information,it may help another person too.
– Dr. Thomas Varughese MS, FICS (Onco) FACS Oncologist & Surgeon (Specialized in Reconstructive Surgery) Kerala
00seshunarayanahttps://imedworks.com/wp-content/uploads/2020/09/MedWorks-Logo-02-300x300.pngseshunarayana2020-08-10 18:27:462020-08-10 18:27:46Things you need to know about Breast Cancer – Dr. Thomas Varughese
A new study analyzes rare tumors in which insulin-producing beta cells are produced in excess in order to find a “genetic recipe” for regenerating these cells. And the findings might change the current therapeutic practices for treating diabetes. Beta cells play a crucial role in the development of diabetes. These tiny cells found in our pancreas produce insulin, and a loss of beta cells is known to be a cause of type 1 diabetes.
Additionally, recent studies have shown that beta cells also play a crucial role in the development of type 2 diabetes. For instance, a study that Medical News Today reported on found that the release of pro-inflammatory proteins kills off insulin-producing beta cells in the early stages of type 2 diabetes.
But the “problem” with beta cells, medically speaking, is that they replicate in early childhood but cease to proliferate after that.
New research, however, carried out by scientists at the Icahn School of Medicine at Mount Sinai in New York City, NY, uncovers a “genomic recipe” for regenerating these key cells.
The study was led by Dr. Andrew Stewart, the director of the Diabetes, Obesity, and Metabolism Institute at the Icahn School of Medicine, and the findings were published in the journal Nature Communications.
Studying rare tumors to fight diabetes For the new research, Dr. Stewart and team analyzed a very rare type of benign tumor called insulinomas. These are “pancreatic beta cell adenomas” that secrete too much of the hormone insulin.
The tumors are small and proliferate slowly. The researchers used whole-exome and RNA-sequencing analysis to examine the genetic makeup of 38 such tumors.
Speaking to Medical News Today about the rationale for choosing to study insulinomas, Dr. Stewart said, “In order to discover drugs that would make human pancreatic beta cells regenerate in people with diabetes, we wanted to understand how human beta cells normally replicate.”
“Unfortunately,” he added, “human beta cells only replicate in the first year of life, so obtaining beta cells from babies is difficult. On the other hand, insulinomas […] are a prefect model: they are rare, they are benign […] tumors of the human beta cell[s], and make large amount of insulin, so much [that] they cause low blood glucose (hypoglycemia).”
00seshunarayanahttps://imedworks.com/wp-content/uploads/2020/09/MedWorks-Logo-02-300x300.pngseshunarayana2020-08-10 18:19:582020-08-10 18:19:58How pancreatic tumors could help to fight diabetes
A new smart bandage may change our wound caring practices. Researchers have designed a “smart” bandage that is much more effective and faster-acting than regular healing patches. The same device can also be loaded with drugs, depending on the type and stage of the wound it is applied to.
The idea for the new device was born out of the need to find more efficient, expedient, and cost-effective treatments for chronic wounds.
Chronic wounds – including venous ulcers, diabetic ulcers, and pressure ulcers – are particularly challenging to treat due to the complex biological mechanism that characterizes them.
They do not heal after the standard 4 weeks of care, largely because the body does not release the compounds that are essential to healing in a timely fashion.
But the new device may change this. Being able to administer different drugs at different stages in the progression of the wound is known to help with chronic wounds, and the smart bandage allows medical professionals to do just that using one single device.
The smart healing patch was engineered by researchers from the University of Nebraska-Lincoln (UNL) in collaboration with scientists from Harvard Medical School in Boston, MA, and the Massachusetts Institute of Technology in Cambridge, MA.
In the new study – which is published in the journal Advanced Functional Materials – the team details a series of experiments that they ran in order to test the benefits of their innovation.
One of the corresponding authors of the study is Ali Tamayol, an assistant professor of mechanical and materials engineering at UNL. “The medical cost associated with [chronic] wounds is tremendous,” he says. “So there is a big need to find solutions for [them].”
How the smart bandage works
The smart healing patch is the size of a postage stamp, made up of electrically conductive fibers, and can be controlled remotely with a smartphone or another wireless or bluetooth device.
The fibers are coated with a water-based gel that can be loaded with various drugs, depending on the needs of the wound. Antibiotics, so-called growth factors that help the tissue to regenerate, and painkillers could all be alternatively administered using the same “e-bandage,” all the while controlling remotely not only the substance, but also the dosage.
In one of the experiments detailed in the study, the researchers applied the e-bandage loaded with a tissue-growth factor to wounded mice, and a normal “dry” bandage to a control group of mice.
The experiment showed that the smart bandage helped the mice to regrow three times as much tissue than the control group did. Tissue regeneration is a key step in the healing process.
In another experiment, the team loaded the bandage with an antibiotic. The smart healing patch successfully fought off the infection.
“This is the first bandage that is capable of dose-dependent drug release […] You can release multiple drugs with different release profiles. That’s a big advantage in comparison with other systems.” Prof. Ali Tamayol “What we did here,” he continues, “was come up with a strategy for building a bandage from the bottom up […] This is a platform that can be applied to many different areas of biomedical engineering and medicine.”
“Imagine that you have a variable patch that has antidotes or drugs targeted toward specific hazards in the environment,” Tamayol adds.
The researchers also hope that the first application of their device will be to heal the chronic ulcers that result from diabetes.
The majority of the bandage’s components have already been approved by the Food and Drug Administration (FDA), the researchers say. But before bringing the device to market, the bandage will still have to be tested in animals and then in human trials.
Until then, the team is hard at work trying to make the bandage capable of administering the appropriate treatments autonomously.
Scientists may have discovered a way of reversing heart failure by getting heart muscle to regenerate itself.They found that silencing a signaling pathway in mice that had developed heart failure following a heart attack activated a previously unrecognized self-healing process.
In a paper recently published in the journal Nature, the researchers, led by a team from Baylor College of Medicine in Houston, TX, report their findings about the signaling pathway, which is known as Hippo.
Heart failure is a serious condition that affects around 5.7 million adults in the United States. It develops when the heart cannot pump enough blood to meet the body’s needs.
Heart failure does not mean that the heart has stopped pumping, but it does mean that vital organs do not get the oxygen and nutrients they need to function properly. Around half of patients with heart failure do not live more than 5 years after diagnosis.
“Heart failure remains the leading cause of mortality from heart disease,” explains corresponding author James F. Martin, a professor who specializes in regenerative medicine at Baylor College of Medicine and who is also director of the Cardiomyocyte Renewal Lab at the Texas Heart Institute, also in Houston.
Injured hearts favor scarring to regeneration
At present, the best treatment for heart failure is a heart transplant. However, the number of heart failure patients far exceeds the number of hearts available for transplant. Having a ventricular assist device implanted is also an option, but it is a much less favorable one.
One of the curious things about heart muscle is that it does not regenerate when it dies after being starved of oxygen, such as after a heart attack.
Instead of generating new beating muscle cells, or cardiomyocytes, the heart replaces the dead tissue with scar tissue made from fibroblast cells. Unlike cardiomyocytes, fibroblasts have no pumping ability, so the heart gradually gets weaker and weaker, with the result that the majority of severe heart attack patients develop heart failure. Prof. Martin says that he and his laboratory team are studying biological pathways that are active during heart development and regeneration in order to find ways to heal heart muscle.
Biological pathways are series of molecular events inside cells that lead to changes in the cell or result in particular products. For example, they can turn genes on and off and they can trigger cells to make fats, proteins, hormones, and other molecules. They can also carry signals and cause cells to move.
Silencing the Hippo pathway
“In this study, we investigated the Hippo pathway, which is known from my lab’s previous studies to prevent adult heart muscle cell proliferation and regeneration,” Prof. Martin notes.
In their study paper, he and his colleagues explain that the Hippo pathway – “a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration” – is more active in patients with heart failure.
“This,” says first author John Leach, a graduate student of molecular physiology and biophysics in Prof. Martin’s group, “led us to think that if we could turn Hippo off, then we might be able to induce improvement in heart function.”
So, the team silenced the Hippo pathway in a mouse model that mimics the type of advanced heart failure that occurs in humans after a heart attack. They compared the results with those of a group of healthy mice (the controls).
“After 6 weeks we observed that the injured hearts had recovered their pumping function to the level of the control, healthy hearts,” says Leach.
The researchers believe that silencing Hippo not only renews heart muscle cells – as investigated extensively in their study – but it also changes the process of fibrosis, or scarring. They call for further studies to investigate the effects on fibrosis.
“Our findings indicate that the failing heart has a previously unrecognized reparative capacity involving more than cardiomyocyte renewal.”
A new type of stem-like heart cell has been transformed into heart muscle, proving that dormant cells exist in the heart that have the capacity to carry out repairs, researchers from University College London reported in the journal Nature. The authors believe hearts damaged by a heart attack might be eventually encouraged to repair themselves.
At the moment there is no way of undoing heart damage caused by myocardial infarction (heart attack). The damage commonly leads to heart failure and poor prognosis – a problem which in the UK alone affects over 750,000 individuals.
The researchers targeted progenitor cells in the outer layer of the heart (epicardium). These EPDCs (epicardium-derived progenitor cells) in the embryo can turn into various types of specialist cells, including heart muscle ones.
Scientists had thought that the ability to transform is lost when the human becomes an adult. The authors explain that they have managed to reactivate this potential.
They treated the healthy hearts of adult mice with thymosin β4 (Tβ4), a peptide molecule, which appeared to prime the heart for repair – restoring the EPDCs’ embryonic potential.
When the heart became damaged, a Tβ4 booster was administered, encouraging the EPDCs to turn into new heart muscle and integrate with existing healthy muscle. The authors stressed that without being pre-treated with Tβ4, muscle is not formed.
Study leader, Professor Paul Riley at UCL Institute of Child Health, said:
“I could envisage a patient known to be at risk of a heart attack – either because of family history or warning signs spotted by their GP – taking an oral tablet, along the lines of a statin, which would prime their heart so that if they had a heart attack, the damage could be repaired.”
It will be several years before humans can be effectively treated in this way, the scientists wrote. Tβ4 only resulted in the generation of a small number of heart muscle cells to be generated.
The British Heart Foundation is funding further research into Tβ4. The aim will be to make it more effective, or perhaps find alternative ways to activate the embryonic potential of EPDCs, and eventually apply what they achieve in animal studies to humans.
Professor Riley said:
“This is an important piece of work and something we’ve been working toward for some time. Our earlier research proved blood vessels could be regenerated in adult hearts but there were major doubts about whether the same might be true for heart muscle. This work has demonstrated a possible method for repairing hearts damaged by a heart attack and could have a major impact on future therapies to treat heart failure.”
Professor Jeremy Pearson, Associate Medical Director at the British Heart Foundation, said:
“To repair a damaged heart is one of the holy grails of heart research. This groundbreaking study shows that adult hearts contain cells that, given the right stimulus, can mobilise and turn into new heart cells that might repair a damaged heart. The team have identified the crucial molecular signals needed to make this happen.
These results strengthen the evidence that in the future there may be a drug, or cocktail of drugs, that could be given to people whose hearts have been damaged by a heart attack, to prevent the onset of heart failure. This is why the BHF has launched its Mending Broken Hearts appeal to raise money for research to turn this vision into reality for heart patients as quickly as possible.”
00seshunarayanahttps://imedworks.com/wp-content/uploads/2020/09/MedWorks-Logo-02-300x300.pngseshunarayana2020-08-07 12:34:082020-08-07 12:34:08Damaged Hearts Could Be Encouraged To Self-Repair
Kale, parsley, broccoli, and spinach: according to new research, these leafy green vegetables may hold even more health benefits than previously thought, as vitamin K – found in abundance in all four – may contribute to a healthy heart. A new study published in The Journal of Nutrition examines the link between vitamin K levels and heart structure and functioning in young people.
Vitamin K plays a key role in blood coagulation and bone health. Deficient levels of the vitamin raise the risk of hemorrhage, osteoporosis, and bone fractures.
In its dietary form, vitamin K is known as phylloquinone, or vitamin K-1. This is abundantly found in leafy green vegetables such as kale, parsley, broccoli, spinach, iceberg lettuce, and cabbage.
The new research suggests that insufficient levels of the vitamin may affect the structure of the heart, leading to a condition called left ventricular hypertrophy (LVH).
The left ventricle is the heart’s major pumping chamber, and in LVH, this chamber is enlarged to an unhealthy degree. As the authors of the new study explain, a larger heart can malfunction with time, becoming less effective at pumping blood.
LVH tends to affect adults, but the researchers decided to study this heart structure in young people because cardiac abnormalities that begin in childhood tend to predict the risk of cardiovascular disease in adulthood.
To the best of the authors’ knowledge, this is the first time that a study has examined links between vitamin K levels and heart structure in teenagers.
Mary K. Douthit and Mary Ellen Fain, both of the Georgia Prevention Institute at Augusta University, are the study’s co-first authors. Dr. Norman Pollock, a bone biologist at the same institute, is the study’s corresponding author.
Low vitamin K-1 intake correlates with LVH The researchers assessed the diet and physical activity habits of these teenagers over a period of 7 days, using the participants’ self-reporting and accelerometry devices. Left ventricular structure and functioning were assessed using echocardiography.
Overall, the study found that the teenagers who consumed the least amount of vitamin K-1 had considerably greater left ventricles compared with those who consumed sufficient amounts of the vitamin.
The researchers divided the results into tertiles, or thirds, of vitamin K-1 intake. They found, “The prevalence of [LVH] progressively decreased across tertiles of phylloquinone intake.”
In other words, the more vitamin K-1 the teenagers consumed, the less likely they were to develop LVH.
Dr. Pollock spoke to Medical News Today about the findings. He said, “[Teens] consuming 42 micrograms per day or less of vitamin K were more than three times [more] likely to have left ventricular hypertrophy than those consuming 90 micrograms per day or more.”
“Strikingly,” Dr. Pollock added, “this relationship persisted even after taking into account potentially confounding factors such as age, sex, race, pubertal stage, blood pressure, body composition, physical activity, and other factors of dietary intake.”
Around 10 percent of the teenagers had LVH to some degree, as determined by measurements of the overall size of the ventricle and the thickness of its walls.
Clinical implications of the findings The findings, the authors write, help them to “clarify the importance of phylloquinone intake to cardiovascular development.”
Speaking to MNT about the clinical implications of the study, Dr. Pollock said that “cardiovascular disease risk factors have been shown to track during childhood and later life and may be affected by dietary intake, [so] it is of clinical relevance to study dietary determinants of cardiovascular development.”
“Our observational data suggest that greater vitamin K consumption may favorably influence subclinical markers of cardiac structure and function in a population of U.S. adolescents.” Dr. Norman Pollock The study authors write that although further research is now needed, the new findings could ultimately “lead to phylloquinone interventions in childhood aimed to improve cardiovascular development and to reduce the subsequent risk of [cardiovascular disease].”
In fact, Dr. Pollock is currently the lead investigator in four vitamin K trials aiming “to determine the effect of vitamin K supplementation on risk markers of cardiovascular disease and diabetes.”
00seshunarayanahttps://imedworks.com/wp-content/uploads/2020/09/MedWorks-Logo-02-300x300.pngseshunarayana2020-08-07 12:27:472020-08-07 12:27:47Leafy greens may contribute to a healthy heart
