Tag Archives: cell

Fuss about food – Omega 3

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fishoil.jpgAfter the big ‘fat is bad’ push of the 1980s and 1990s, we are finally coming around to the idea that some fats are good for us.

But which ones?

The good ones are Polyunsaturated fats (PUFAs) and Monounsaturated fats (MUFAs).

Omega 3 and 6 fats are PUFAs and are classed as essential.
Our bodies cannot manufacture these so we need to make sure we are eating foods which contain them.

It seems like every day we hear about something else that we should be eating or drinking. So what makes Omega 3 special?

We need good fats for a whole host of things – every cell in your body relies on fat to survive. They are essential for nerve, heart and brain health and for nearly all of the body’s basic functions.

We seem to have no problem getting enough Omega 6 fat but there is one big catch – Omega 6 fats are dependent on Omega 3 to produce optimal health benefits and are only considered good fats when consumed in moderation.

Omega 3 fats have an amazing role in your body as an anti-imflammatory. Consuming them reduces your risks of developing heart disease, arthritis and cancer. It is widely acknowledged to have a pivotal role in the prevention of heart disease.

Omega 6 fats, while helpful in reducing bad cholesterol, can promote inflammation within our bodies when too much is consumed – a very undesirable quality. The developed world, as a whole, is extremely inflamed.

In the US, diets tend to contain up to 25 times more Omega 6 than Omega 3 fats.

Mediterranean diets have long been studied to identify exactly what promotes heart health and longevity. These studies have indicated that it is the healthy balance between Omega 3 and 6 fatswhich leads to a longer and healthier life.

People who follow such a diet are much less likely to develop heart disease. The mediterranean diet traditionally contains much reduced levels of meat consumption, which is a major source of omega 6 fats. It focuses on foods rich in omega 3 fats, including wholegrains, fresh fruit and vegetables, garlic, fish and olive oil. Moderate intake of wine also adds something to the balance.

If you only take one supplement a day, health professionals are almost all in agreement that it should be a fish oil supplement.

Clinical evidence suggests that EPA and DHA (eicosapentaenoic acid and docosahexaenoic acid, the two omega-3 fatty acids found in fish oil) help reduce risk factors for heart disease, including high cholesterol and high blood pressure. Fish oil has been shown to lower levels of triglycerides (fats in the blood), and to lower risk of death, heart attack, stroke, and abnormal heart rhythms in people who have already had a heart attack.

If you are sceptical about the importance of these fats, consider the symptoms of someone suffering from a defiency in Omega 3; tiredness, poor memory, dry skin, heart problems, mood swings, depression and poor circulation.

Omega 3 fats are highly concentrated in the brain and appear to be important for cognitive (brain memory and performance) and behavioral function. So if you feel like you need a memory or energy boost, you could find your answer in changing your diet just a little bit.

If you are on blood thinners or diabetes medication, you should consult your GP before starting to take fish oil supplements.

Later this week we will be examining a sinner of the fat world – Trans fats.

Can infra red light grow new brain cells to reverse Alzheimer’s?

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London: A scientist has claimed that an experimental helmet whch bathes the brain in infra-red light is capable of stimulating the growth of new brain cells in patients with Alzheimer’s disease.

The creators of the helmet, a County Durham, UK-based medical research company called Virulite, say that ten minutes use daily over a period of four weeks can reverse the symtoms of dementia.

Dr Gordon Dougal, a director of Virulite, bases the claims on a study at the University of Sunderland which found infra-red light can reverse memory loss in mice.

Dr Dougal says that the treatment not only stops brain decay but partially reverses it.

The study at Sunderland found that exposing middle-aged mice to infrared light for six minutes a day for ten days improved their performance in a three-dimensional maze. In the human trials, due to start this summer, the scientists will use levels of infra-red that occur naturally in sunlight.

Bones act as an organ – new research reveals

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Even though bones seem to be metabolically inactive structures, nothing could be further from the truth. In fact, bones are rebuilt constantly through the action of cells known as osteoblasts while old bone is destroyed by other cells known as osteoclasts. Bones also produce red and white blood cells, help maintain blood pH and store calcium.

However, exciting new research published in this month’s edition of the magazine Cell, has shown that bones also act as an endocrine organ. Not only do bones produce a protein hormone, osteocalcin that regulates bone formation, but this hormone also protects against obesity and glucose intolerance by increasing proliferation of pancreatic beta cells and their subsequent secretion of insulin. Osteocalcin was also found to increase the body’s sensitivity to insulin and as well as reducing its fat stores.

Hormones function as chemical messengers that allow the body to precisely coordinate metabolism, reproduction and other essential biological processes that involve multiple organs.

“The skeleton used to be thought of as just a structural support system. This opens the door to a new way of seeing the bones,” said Dr. Gerard Karsenty, chairman of the department of genetics and development at Columbia University Medical Center in NYC, who headed the team that made the discovery.

Osteocalcin is not new to science: Its existence has been known for 50 years, “but its function was never understood,” observed Karsenty. However, researchers have long known that people with diabetes tend to have low levels of osteocalcin, but until now no one understood the significance.

Based on their knowledge of skeletal biology and endocrinology, the research team hypothesized that there might be a relationship between skeletal biology and endocrine regulation because of the long-known observation that obesity protects against osteoporosis in mammals. Additionally, it was known that people with untreated type 2 diabetes have low osteocalcin levels, which made this hormone an appealing target for their research efforts.

To do this research, the scientists designed an elegant series of experiments using several groups of mice. The first group of experimental mice had their osteoblast gene, called Esp, genetically deactivated, or “knocked out”. Esp encodes a receptor-like protein tyrosine phosphatase called OST-PTP that increases beta-cell proliferation and insulin secretion in the pancreas, which results in hypoglycemia. But these so called “knock-out mice” lacked all functional Esp genes, so their insulin secretion and sensitivity decreased causing them to become obese and then to develop Type 2 diabetes when fed a normal diet. Type 2 diabetes occurs when the body becomes resistant to insulin, the hormone that regulates sugar metabolism.

A second group of experimental mice were genetically engineered to over-produce osteocalcin. These mice showed lower-than-normal blood glucose levels and higher insulin levels than did normal mice that were fed a normal diet. Additionally, these “overproducer mice” also showed increased insulin sensitivity. This is probably the most exciting result because typically, excess blood insulin decreases tissues’ sensitivity to the hormone, which makes insulin treatment difficult for diabetics. Further, the team found that treating the “knock-out mice” with osteocalcin helped regulate their blood sugar and insulin.

Additionally, the investigators reported that mice with one functional copy of Esp showed a significant reversal of their metabolic abnormalities, which provides “genetic evidence that Esp and osteocalcin lie in the same regulatory pathway and that [the] Esp-/- mice metabolic phenotype is caused by a gain-of-activity of this hormone.”

Interestingly, mice that are genetically programmed to overeat and mice that were fed fatty diets were prevented from suffering both obesity and diabetes when given high levels of osteocalcin. Karsenty is now determining whether giving osteocalcin to his diabetic “knock-out mice” will reverse the disease. This research shows promise for treating human diabetics as well.

Finding a substance that increases beta cell proliferation, says Karsenty, “is a holy grail for diabetes research.” Thus, if what’s true for mice also proves true for humans, “then we have inside us a hormone that does precisely this.”

“The findings could have important implications for the treatment of diabetes. Osteocalcin has a triple-punch effect, in that it raises both insulin levels and insulin uptake while keeping fat at bay. That makes it a promising therapy for middle-aged people who want to fight type 2 diabetes,” Karsenty said.

Additionally, this study also reveals that the skeleton is an important part of the endocrine system.

“To our knowledge this study provides the first in vivo evidence that [the] skeleton exerts an endocrine regulation of energy metabolism and thereby may contribute to the onset and severity of metabolic disorders,” the authors wrote in their paper.

Gene trigger for stem cell shut down in ageing

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Biologists have uncovered a gene that shuts down stem cells as people age.

They say the gene known as p16-Ink4a gradually reduces the ability of stem cells to proliferate, thus reducing the risk of cancer.

The discovery, reported in the scientific magazine Nature, was made in an experiment on mice, but the scientists believe that it applies to humans too.

The finding indicates that many degenerative diseases of ageing are caused by an active shutting down of the stem cells that renew the body’s various tissues and are not just a passive disintegration of tissues under daily wear and tear.

Senior author Dr Norman E Sharpless of the University of North Carolina said: “I don’t think aging is a random process — it’s a program, an anticancer program.”

The finding that stem cells are switched off with age is not encouraging for those who wish to use a patient’s own adult stem cells to treat disease.

The gene plays a central role in the body’s defenses against cancer, and it produces two quite different proteins that interact with the two principal systems for deciding whether a cell will be allowed to divide.

One of the proteins had also been noted to increase substantially with age. The cells of a 70-year-old produce 10 times as much of the Ink4 protein as those of a 20-year-old.

In the experiment the scientists genetically engineered a mouse strain with the gene knocked out. They found that the mouse cells had an extra ability to proliferate when the Ink4 protein was not present. At the same time the mice were highly prone to cancer which they developed as early as a year.

The researchers assume, but have not yet proved, that the increasing amounts of Ink4 as a person ages will thrust the stem cells into senescence, meaning that they can never divide again. The evolutionary purpose is evidently to avert the risk that a damaged stem cell might evade controls and proliferate into a tumor.

One implication is that therapists who hope to increase longevity have to tackle a system that may be hard to cheat. An intervention that reduces Ink4 production to prevent the age-related decline of stem cells will also increase the risk of cancer.

Dr Sharpless said that so far the only intervention known to increase lifespan was a calorically restricted diet which also reduced cancer, at least in laboratory mice. The reason, he said, is probably because such diets reduce cell division, the prime source of cancer risk.

For cell therapists, the dual activity of Ink4 may be “a hard box to get out of,” he said, unless they use cells that are somehow much younger than the patient.

Some proposals for stem cell therapy with adult stem cells envisage taking a patient’s stem cells, making them divide in the laboratory and putting them back in the patient to build new tissue.

The researchers said they did not yet know what stimulus makes cells increase their production of the Ink4 protein as a person grows older. Their suspicion is that the usual factors implicated in aging like mutation and oxidative damage to tissues would turn out to have a role in making cells produce more Ink4.