Medi-Tech will bring to the table win-win strategies to ensure proactive domination. Working with Doctors and other medical offices to help their patients have a more seamless doctor-patient visit or interaction.

Medi-Tech, Inc. efficiently unleashes products and services information to all of our clients making sure all of our clients are aware of the value we are offering. We at Medi-Tech, Inc. quickly maximize timely deliveries for real-time quick results and to dramatically maintain profitable solutions without sacrificing functional solutions.

Completely synergize resource taxing relationships via premier niche markets. Professionally cultivate one-to-one customer service with robust ideas. Dynamically innovate resource-leveling customer service for state of the art customer service.

Vitamin D is a vital nutrient, helping the gut to absorb calcium while keeping calcium and phosphate at the right concentrations to support healthy bone growth and maintenance. Without adequate levels in the body, bones can become brittle and misshapen.

Low vitamin D levels have also been linked with a range of other conditions, including cardiovascular disease and cancer.

Vitamin D is not naturally present in many foods. Instead, the bulk of our requirement is synthesized in the skin after exposure to ultraviolet light from the sun.

Despite the importance of vitamin D, many people in the United States do not have sufficient levels in their bodies. For example, one study found that overall, more than 40 percent of the U.S. population were vitamin D deficient. So much so, that some authors have referred to vitamin D deficiency as a pandemic.

Furthermore, in one study published in 2009, only 3 percent of black people in their sample of thousands of U.S. individuals had the recommended vitamin D levels, representing a decrease of 9 percent over the previous 20 years.

For this reason, it is becoming increasingly important to understand how the vitamin works and to ensure that the right type of supplements are reaching individuals most at risk.

Not all vitamin D types are equal

There are two types of vitamin D, which are known as D-2 and D-3. The former is derived from plant sources, particularly fungi, while the latter comes from animal sources.

The two types of vitamin D are very similar, differing only in the structure of their side-chains, and it is generally accepted that both perform similarly well as a supplement. In fact, on the National Institutes of Health website, they write, “The two forms have traditionally been regarded as equivalent.”

Researchers from the University of Surrey in the United Kingdom recently set out to test whether or not this widely held belief is correct. They wanted to understand which of the two nutrients raises levels of vitamin D in the body most effectively.

The researchers measured vitamin D levels in 335 South Asian and white European women over two winter periods. They chose winter because, due to a reduction in sunlight exposure, vitamin D levels tend to be lower at this time.

The women were split into five groups: those consuming vitamin D-2 in a biscuit; those consuming vitamin D-3 in a biscuit; those consuming vitamin D-2 in a juice drink; those consuming vitamin D-3 in a juice drink; and those receiving a placebo.

The study found that vitamin D-3 was twice as effective at raising vitamin D levels in the body as vitamin D-2.

Participants who received the D-3 in a biscuit raised their levels of vitamin D by 74 percent, while those receiving the vitamin in juice saw a 75 percent increase. Those receiving D-2 had a 33 and 34 percent increase, respectively. The placebo group experienced a drop of 25 percent across the same period.

Changes to guidelines and products

These findings have implications for the medical community, of course, but they also impact the retail sector; many companies add vitamin D-2 to beverages and foods. Some may therefore now want to think their choices.

As lead author Dr. Laura Tripkovic says, “The importance of vitamin D in our bodies is not to be underestimated, but living in the U.K., it is very difficult to get sufficient levels of it from its natural source, the sun, so we know it has to be supplemented through our diet.” The same can be said for many parts of the U.S.

She continues, “[O]ur findings show that vitamin D-3 is twice as effective as D-2 in raising vitamin D levels in the body, which turns current thinking about the two types of vitamin D on its head.”

“Those who consume D-3 through fish, eggs, or vitamin D-3-containing supplements are twice as likely to raise their vitamin D status than when consuming vitamin D-2-rich foods, such as mushrooms, vitamin D-2-fortified bread, or vitamin D-2-containing supplements, helping to improve their long term health.”

– Dr. Laura Tripkovic

Vitamin D deficiency appears to be widespread, and, as more research is conducted, it becomes increasingly clearer that this nutritional deficit is having a significant impact on the health of the country overall. Studies such as this may play a role in improving awareness, and, eventually, reversing the trend.

In a paper published in Cell Reports, researchers from Imperial College London in the United Kingdom and INSERM UMRS 1138 in Paris, France, among others, describe how they used genetically similar mice to show that gut microbes influence the body’s response to changes in diet and affect health.

If further research finds that the effect is also true of humans, the researchers believe that it could lead to doctors prescribing personalized diets for patients based on the unique composition of their gut flora.

“We know that our environment and genetics can influence our risk of obesity and disease, but the effects of these communities of bacteria living inside us are less well understood,” says study leader Dr. Marc-Emmanuel Dumas, a reader in transnational systems medicine at Imperial College London.

Gut microbiome, health, and diet

The human gut, which represents one of the largest interfaces between the body and the environment, is home to vast colonies of bacteria and other microbes that have co-evolved with their hosts over thousands of years to play a vital role in health and disease.

From the day we are born, our gut microbiome – that is, the collection of gut microbes and their genetic material – is not only helping to digest food and make vitamins, but it is also shaping our immune system and the way our body responds to agents of disease.

Scientists are also starting to uncover a vast and complex system through which gut microbes might influence human brain development and behavior through their metabolites, the chemical byproducts of their activity.

It has also been established that diet is one of the main factors in shaping the gut microbiome over the course of life.

Now, Dr. Dumas and colleagues also show that there could be an effect in the other direction: that the gut microbiome may determine how the body responds to diet.

Gut microbiome predicts diet effects

For their study, the researchers placed around 50 mice with similar genetic makeup on a high-fat diet and tracked changes in their health and behavior.

Before switching the mice to the high-fat diet, the team used magnetic resonance spectroscopy to screen urine samples from the animals for metabolites of their gut microbes. This yielded a “gut microbiome signature” for each animal.

The high-fat diet resulted in several changes in the mice, but not all of them were affected in the same way, despite the fact that they were genetically similar.

Some mice put on more weight than others, and some became less tolerant of glucose. Glucose intolerance is an early sign of diabetes. There were also some changes in behavior, such as in levels of anxiety and activity.

Analysis against the animals’ gut microbiome signatures showed that they were predictive of some of the changes. The team found that one metabolite in particular, called trimethylamine-N-oxide, was an accurate predictor of glucose intolerance.

Co-senior author Jeremy K. Nicholson, a professor and head of the Department of Surgery and Cancer at Imperial College London, explains that in early life, “we start off with very few bugs” and our microbiome enlarges as we acquire more microbes from our environment.

“This means that small differences in the local environment can result in a great diversity in terms of the microbiome,” he adds, as he sums up the research:

“This study is another fascinating example of the power of the microbiome to influence the host with respect to major health risks. It shows that value of a diet is determined not only by your genes, but also the genes of your gut microbes.”

According to the American Cancer Society, around 53,070 people will be diagnosed with pancreatic cancer in the Unites States in 2016, and around 41,780 people will die of the disease. Pancreatic cancer accounts for about 3 percent of all cancers in the U.S. and about 7% of cancer deaths.

Pancreatic cancer is caused by the abnormal, uncontrolled growth of cells in the pancreas.

A research team at Cold Spring Harbor Laboratory (CSHL) in New York finds that reducing levels of antioxidants in pancreatic cells can help to kill them. This new strategy for eradicating pancreatic cancer cells may open new doors for treating this serious illness, in which less than 5 percent of patients survive 5 years.

“Antioxidant” has become a popular buzzword that is viewed as a cure-all notion for health ailments; it is widely believed that raising levels of antioxidants stops cancer cells from developing.

In reality, although antioxidants interact with and neutralize free radicals and prevent them from causing damage, there is little available evidence that antioxidants prevent cancer.

Furthermore, trials have found that people taking antioxidant supplements during cancer therapy have worse outcomes, especially if they were smokers.

Does increasing antioxidant levels do more harm than good?

In a series of complex experiments, the CSHL researchers demonstrate that in pancreatic cells that are abnormal or in a malignant state, raising antioxidant levels can do more harm than good.

In healthy cells, the amounts of oxidizing and anti-oxidizing agents are kept precisely balanced in every cell.

However, in proliferating cancer cells – that are increasing rapidly in number through growth and cell division – the amounts of oxidants in malignant cells increase, but anti-oxidants also increase to counter the impact of rising oxidation.

CSHL’s Prof. David Tuveson – M.D., Ph.D., director of research for the Lustgarten Foundation – and colleagues note that without the amounts of antioxidants going up in scale with the oxidants, malignant cells will die from excessive oxidation.

“Of course, that’s exactly what we want cancer cells to do – to burn themselves out,” says Iok In Christine Chio, a postdoctoral investigator in the Tuveson lab who led the experiments.

“The therapeutic principle our lab is testing is whether, by increasing the level of oxidation in cancer cells, we can cause pre-malignant and malignant cells to die,” she adds.

Excessive oxidation causes cells to commit suicide

Treatments for cancer such as radiation therapy and chemotherapy destroy cancer cells by promoting oxidation. Although antioxidants protect cellular DNA from damage by oxidation stress, they likely protect cancer cells, too.

Exposing cells to excessive oxidation causes them to experience programmed cell death called apoptosis. A method of increasing oxidation in cancer cells is to decrease levels of antioxidants within the same cells.

Tuveson and team aimed to find a technique whereby they could increase oxidation without harming healthy cells. They concentrated on NRF2, a protein that can be tweaked to disrupt the balance between oxidation and decreased cancer cells.

When NRF2 is active, cells synthesize a chemical called glutathione, an important antioxidant. However, it is not possible to reduce NRF2 activity or make it inactive, as it has a role in regulating several hundred different genes. “One can’t delete it from a cell without impacting many other processes,” says Chio.

The team used samples of pancreas cells from people with pancreatic cancer (malignant and pre-malignant) and individuals with a healthy pancreas to conduct an experiment where NRF2 was eliminated.

Normal pancreas cells not harmed by two-drug treatment

They found that when NRF2 was missing, the process of translating messages from the genes into proteins was highly affected by the oxidant and antioxidant balance, but only in the cancerous cells. The healthy cells were still able to produce the proteins.

“We were very excited when we saw this. This meant that if we could find a way of reducing antioxidants, protein synthesis would only be impacted in precancerous and malignant cells, a potentially powerful therapeutic strategy.”

Iok In Christine Chio, postdoctoral investigator, Tuveson Lab

The crux of the experiment was to use two drugs in combination: an AKT (protein kinase B) inhibitor, and a BSO (buthionine sulfoximine), which reduces levels of glutathione.

AKT inhibitors have been used in trials on cancer patients before but with limited success. The team wanted to combine this with the BSO to mimic what would happen if they could reduce levels of NRF2.

“We were able to test this idea and see that this approach was synthetically lethal – it did increase the killing power of the AKT inhibitor, but the synergy was not present in the setting of normal pancreas cells,” Chio says. Fundamentally, healthy pancreas cells were not damaged by the treatment.

The team hopes their findings can enable them to propose new treatments and approaches for cancer patients, and they hope to start clinical trials in the near future.

Chili peppers contain a chemical compound called capsaicin, which is part of a group of chemicals that give chilies their individual taste and heat profile. Capsaicin can activate neurons in the diaphragm, which contracts and causes hiccups.

Capsaicin is also an irritant. Chili plants are thought to use capsaicin as a defense mechanism in order to stop animals from eating the plant. In fact, humans are the only species known to enjoy eating spicy food.

Chili peppers and pain

Capsaicin binds to a pain receptor called TRPV1. When we accidentally expose our skin or eyes to chilies, we activate TRPV1 receptors, thereby causing the pain floodgates open. These receptors in our mouths are the reason for the “mouth-on-fire” feeling we experience when we eat spicy food.

Interestingly, once a pain receptor is stimulated by capsaicin, it goes into a period of rest, which means that the same receptor doesn’t transmit pain signals again.

Scientists call this process “defunctionalization.” This is why capsaicin is used to treat pain in some patients; it leads to loss of pain perception.

The capsaicin receptor is found throughout the body, including in the nerves that control our diaphragm, which is the muscle that allows our lungs to take in air.

Hiccups are thought to be caused by an involuntary contraction, or spasm, of the diaphragm, followed by contraction of the glottis. Airflow into the windpipe becomes temporarily blocked. When incoming air strikes the glottis, the characteristic hiccup sound occurs.

Scientists are still speculating about the precise mechanism responsible for hiccups, as well as how exactly capsaicin leads to spasms of the diaphragm, which, at this point, remains unclear.

Luckily, the capsaicin molecules that we eat in food don’t stick around for very long; they are rapidly absorbed in the stomach and intestine to be broken down.

But why do some of us start to hiccup at the mere sight of a chili, while others don’t seem to be bothered by spicy foods at all?

Nature, nurture, and the chili response

A Finnish study showed that our preference for spicy food is partly determined by our genes. Differences in number and distribution of capsaicin receptors in our mouths also contribute to our responsiveness to spicy food.

It is, of course, possible to build up a tolerance to chili peppers. There are no definitive scientific studies on human subjects yet, but we can speculate that the mechanism of tolerance occurs through repeated exposure to capsaicin. This will defunctionalize the TRPV1 receptors in the mouth, allowing us to get used to eating spicier food.

A paper on the work – led by the University of California-San Francisco (UCSF) and the University of Washington Medical Center in Seattle – is published in the journal Cell Metabolism.

The researchers believe that the discovery may lead to new obesity drugs that avoid many of the side effects associated with those currently approved for clinical use.

Co-senior author Suneil Koliwad, an assistant professor of medicine at the UCSF Diabetes Center, says that their findings suggest that microglia might be “an untapped and completely novel way to target the brain in order to potentially mitigate obesity and its health consequences.”

Microglia account for 10 to 15 percent of the cells in the brain and spinal cord. They are not the same as neurons, which are brain cells that communicate with each other using electrical and chemical signals.

Microglia are immune cells that play an important role in brain infection and inflammation.

Scientists are beginning to discover that these cells are highly active, even in the resting healthy brain. They are in constant motion, carrying out surveillance and triggering a wide range of responses.

High-fat diets increase microglia

It is coming to light that microglia also influence brain circuit activity during normal conditions. For example, during brain development, they help to shape brain circuits that are important for behavior and response to disease. In the mature brain, they can influence the activity of neurons.

It was already known that a group of neurons in the mediobasal hypothalamus help to regulate the amount of food we eat and how much energy we use.

Under normal conditions, this portion of the brain tries to balance our energy needs with the amount of calories we ingest from food and keep our weight healthy. However, researchers have discovered that eating fat-rich foods can disrupt this balancing process.

Previous research has shown that mice fed fat-rich diets eat more, burn fewer calories, and put on more weight than equivalent mice fed low-fat diets. Fat-rich diets also increase the number of microglia and inflammation in the mice’s mediobasal hypothalamus.

Prof. Koliwad and colleagues wanted to find out whether it is the increase in microglia that causes the overeating and weight gain, or whether it is the weight gain that increases the number of microglia.

Microglia-induced inflammation

The researchers ran an experiment wherein they put two groups of mice on a fast-food, fat-rich diet for 4 weeks. At the same time, one group of mice was treated with a drug that reduced the microglia in their mediobasal hypothalamus, while the other was not.

The results showed that the mice treated with microglia-reducing drug ate 15 percent less food and put on 20 percent less weight than the untreated group fed the same fatty diet.

This suggested that it was the increase in microglia that caused overeating and weight gain. However, it was still not clear whether or not this was due to the microglia triggering inflammation. Thus, the researchers conducted further experiments to find out.

They genetically engineered mice so that their microglia could not trigger immune responses. When fed the fatty diet, these mice ate 15 percent less food and gained 40 percent less weight than normal mice. This suggested that it was the ability of the microglia to trigger inflammation that caused it.

The researchers confirmed this in another group of mice that had been genetically engineered so that their microglia triggered inflammation in response to a drug.

They found that even when these mice were fed a healthful, low-fat diet, giving them the drug triggered their microglia to induce inflammation in the hypothalamus. This caused the treated mice to eat 33 percent more food, use 12 percent less energy, and put on four times more weight than untreated mice on the same diet.

Similar drug already in human trials

The authors note that a drug currently undergoing human trials for the treatment of leukemia, other cancers, and arthritis acts in the same way as the drug that they used to reduce microglia in the mice. They are watching with interest to see if the drug causes the patients in the trials to lose weight.

The team also discovered that when the mice were fed the fat-rich diet, their microglia recruited extra immune cells from the bloodstream.

These blood-borne immune cells not only joined their cousins in the hypothalamus, but they also underwent changes that made them act in a similar way, increasing their inflammation response as well as their influence on energy balance.

The researchers say this suggests that there might be more than one way to influence the microglia to prevent weight gain: through one target in the brain and another target in the bloodstream.

Recent imaging studies show that, compared with slim people, obese people are more likely to have increased numbers of glial cells – the class that microglia belong to – in their hypothalamus. This localized increase of glial cells, called gliosis, is often seen in brain trauma, brain infection, brain cancer, and neurodegenerative diseases.

Ancient survival advantage

Speculating on why glia and microglia might behave in this way, Prof. Koliwad says that the answer might lie in evolution. Perhaps the response is an ancient survival mechanism that was effective in an era wherein energy-rich food was scarce, ensuring that people stored up reserves for leaner times by increasing their appetite.

“Microglial responsiveness to dietary fats makes some sense from this evolutionary perspective. Fats are the densest form of calories that ancient humans might ever [have] had the opportunity to consume,” he explains.

But in today’s modern world, in which high-fat foods are constantly available, the ancient survival advantage has become a disadvantage that can harm rather than preserve life.

Modern humans are more likely to overeat high-fat foods all the time, rather than once in a while. This causes the microglia trigger to be permanently on, leading to increased appetite and a vicious cycle of increasing intake of high-fat food.

The team now plans to investigate in more detail the mechanism through which eating fat-rich foods activates the microglia.

“From these experiments, we can confidently say that the inflammatory activation of microglia is not only necessary for high-fat diets to induce obesity, but also sufficient on its own to drive the hypothalamus to alter its regulation of energy balance, leading to excess weight gain.”

Co-senior author Prof. Joshua Thaler, University of Washington Medical Center

Among many other benefits, the Mediterranean diet has been shown to lower the risk of colorectal cancer. But the specifics of this beneficial role have not been studied in depth.

New research – presented at the ESMO 19th World Congress on Gastrointestinal Cancer, held in Barcelona, Spain – singles out the few components of the Mediterranean diet key for preventing colorectal cancer. The first author of the study is Naomi Fliss Isakov, Ph.D., of the Tel-Aviv Medical Center in Israel.

More specifically, the research looks at the link between the components of the diet taken both separately and in combination, as well as the risk of developing advanced colorectal polyps.

Colorectal cancer tends to develop from advanced polyps, or adenoma. However, the chances of polyps becoming malignant depend on various factors, including size, structure, and location.

Zooming in on the Mediterranean diet

Dr. Isakov and team examined 808 people who were undergoing either screening or diagnostic colonoscopies.

The participants were aged between 40 and 70 years old and were not at a high risk of colorectal cancer. The researchers took anthropometric measurements – such as body mass index (BMI) and height – of the participants, and they asked them to fill in a food frequency questionnaire. They also took part in a medical and lifestyle interview.

The researchers defined adherence to the Mediterranean diet as an above-average consumption of fruit, vegetables, nuts, seeds, and whole grains, as well as fish and poultry.

A below-median intake of red meat, alcohol, and soft drinks was also considered to be a key component of the diet. A Mediterranean diet was also described as having “a high ratio of monounsaturated to saturated fatty acids.”

For the purposes of the study, the researchers defined advanced polyps as adenomas larger than 10 millimeters in size, with a “high-grade dysplasia or villous histology.”

As the American Cancer Society (ACS) explain, the term “dysplasia” refers to the abnormal aspect of the polyps. “High-grade dysplasia” is a term used to describe polyps that appear abnormal or cancer-like. The ACS also note that larger adenomas tend to have a villous growth pattern and are more likely to lead to cancer.

Dr. Isakov and colleagues also examined healthy controls who did not have any polyps, either in the past or at the time of the study.

More fish, fruit reduces risk

Having compared individuals with polyp-free colonoscopies and those whose colonoscopy showed advanced polyps, the authors found a clear association between components of the Mediterranean diet and the risk of colorectal cancer.

People with advanced polyps reported consuming fewer elements of the Mediterranean diet. More specifically, the average was 1.9 Mediterranean diet components in the advanced polyps group, compared with 4.5 components in the polyp-free group.

Surprisingly, even two or three elements of the diet correlated with a 50 percent reduction in the risk of advanced polyps, compared with consuming no key components at all.

Additionally, the risk further decreased as the number of Mediterranean elements increased. The more elements of the Mediterranean diet people consumed, the lower were the chances of advanced polyps showing up in their colonoscopies.

The researchers adjusted for other risk factors associated with colorectal cancer and found that increased fish and fruit consumption, together with a low intake of soft drinks, was most likely to reduce the risk of advanced polyps.

“We found that each one of these three choices was associated with a little more than 30 percent reduced odds of a person having an advanced, pre-cancerous colorectal lesion, compared to people who did not eat any of the MD [Mediterranean diet] components.”

Naomi Fliss Isakov, Ph.D.

She concluded, “Among people who made all three healthy choices the benefit was compounded to almost 86 percent reduced odds.”

ESMO spokesperson Dr. Dirk Arnold, of the Instituto CUF de Oncologia in Lisbon, Portugal, also comments on the findings, saying, “This large population-based cohort-control study impressively confirms the hypothesis of an association of colorectal polyps with diets and other lifestyle factors.”

“This stands in line with other very recent findings on nutritive effects, such as the potential protective effects of nut consumption and vitamin D supplementation which have been shown earlier this year.”

“However,” adds Dr. Arnold, “it remains to be seen whether these results are associated with reduced mortality, and it is also unclear if, and when a dietary change would be beneficial.”

Next, the authors plan to investigate the effects of the Mediterranean diet in a group at high risk of developing colorectal cancer.