Fatty acid

Health myth busted! Low-fat dairy promotes weight gain, heart disease and diabetes

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There’s a reason why many of the people you see regularly guzzling down diet sodas and opting for low- or fat-free dairy when they order their morning lattes are some of the most overweight, unhealthy people in society. Dairy products that have been stripped of their natural fats and fatty acid profiles not only promote unhealthy weight gain but also increase a person’s risk of developing heart disease, diabetes and other related ailments.

fat

Believe it or not, the ridiculous “fat makes you fat” myth is still surprisingly prevalent in many segments of society. Many old-school doctors and dietitians, for example, still actively encourage their patients to eat plenty of whole grains and avoid saturated fats, two grossly ill-advised recommendations that will continue to make people fat and ill until this flawed ideology is completely and forever tossed into the dustbin of bad science.

But this will only happen through continued education on the latest science, which is abundantly clear on the matter. As highlighted by Dr. Chris Kresser on his blog, a series of recent studies conclusively shows that consumption of low- and non-fat dairy products encourages the formation of metabolic disease and everything that it entails, including obesity, high cholesterol, insulin resistance, diabetes and heart disease.

A meta-analysis of 16 studies, in fact, co-authored by Dr. Stephen Guyenet, one of Dr. Kresser’s colleagues, found that all of these risk factors are directly associated with low- and non-fat dairy consumption. Conversely, full-fat dairy consumption was found to be associated with a decreased risk of all of these conditions.

Your body needs unique fatty acids, nutrients found in dairy fat

By removing the fat from dairy products, food processors end up removing a host of fatty acids and other nutrients along with it. These vital constituents not only aid in the digestion and assimilation of other dairy components like whey but also supply the body with necessary protection against gut and cardiovascular degradation.

Butyrate, for instance, one of the primary fatty acids found in dairy fat, provides energy to the cells lining the colon and helps inhibit inflammation in the gastrointestinal tract. In trials, Crohn’s disease patients who dosed 4 grams of butyrate daily for eight weeks were completely cured — butyrate isn’t found in non-fat dairy products.

Another study looking at trans-palmitoleic acid, another prominent fatty acid found in dairy fat, determined that this nutrient is essential in regulating blood cholesterol levels. Trans-palmitoleic acid also helps modulate healthy insulin levels and insulin sensitivity, reducing the risk of diabetes and metabolic syndrome.

Similar benefits are gained from phytanic acid and conjugated linoleic acid (CLA), two other fatty acids in dairy fat. The former was shown to reduce triglyceride levels, improve insulin sensitivity and improve blood sugar regulation, while the latter has been shown to reduce the risk of heart disease, cancer and diabetes.

Full-fat dairy isn’t for everyone, but many people benefit from it

While some people still contend that animal dairy is for baby animals and isn’t intended for human consumption, it is important to remember that everybody’s body is different. Some people require a boost in vitamin K2, for instance, which is only really found in high amounts in full-fat dairy. Dairy fat is also an excellent source of healthy saturated fats when it comes from organic, grass-fed animals treated humanely.

“[D]airy fat is also a good source of fat-soluble vitamins like retinol (active vitamin A) and vitamin K2, which are difficult to obtain elsewhere in the diet,” wrote Dr. Kresser.

Sources:

http://chriskresser.com

http://www.npr.org

http://www.hsph.harvard.edu

Learn more: http://www.naturalnews.com/048079_low-fat_dairy_weight_gain_heart_disease.html#ixzz3Mje3oAAq

Human Breast Milk Inactivates Hepatitis C Virus Infectivity.

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 A new study shows why breastfeeding is generally safe even when mothers are infected with the hepatitis C virus (HCV).

The reason is that human breast milk inactivates hepatitis C virus (HCV) infectivity by disrupting its envelope, researchers from Germany have found.

“This study provides a novel mechanism for the protective properties of human mother’s milk against HCV,” Dr. Eike Steinmann from the TWINCORE Center for Experimental and Clinical Infection Research in Hannover told Reuters Health by email. “A new finding is that lipases in human milk generate free fatty acids that damage the viral envelope and render them non-infectious.”

In an editorial published with the paper online September 24 in The Journal of Infectious Diseases, Dr. Ravi Jhaveri from the University of North Carolina in Chapel Hill says “the results provide a plausible explanation for why breastfeeding is not a risk factor for HCV transmission. This is reassuring for us as practitioners when we counsel our HCV patients that it is safe for them to breastfeed.”

Using breast milk from healthy HCV-negative women, the research team found that even short preincubation periods of HCV in the milk brought consistent reductions of HCV infectivity by 2 to 3 orders of magnitude.

The breast milk inactivated HCV infectivity independent of the viral genotype, and antiviral activity was concentration dependent. Concentrations between 4% and 6% milk were sufficient to reduce HCV infectivity, whereas higher dilutions abolished the antiviral effect.

The antiviral activity was specific to human milk. It was not found in milk from horses, cows, or commercial infant formula.

The anti-viral activity was not destroyed by heat treatment, the authors reported.

In a series of experiments, the researchers showed that lipases in human milk generated fatty acids that disrupted the viral envelope, resulting in the loss of viral infectivity.

“Similar processes concerning the release of free fatty acids take place upon digestion of human breast milk by the infant,” the investigators note. “Therefore, milk digestion products, like free fatty acids, released in the stomach might be able to inactivate residual viral particles which otherwise could be transmitted upon breastfeeding.”

Human breast milk also had significant antiviral effects against other enveloped viruses (influenza, herpes simplex, and vesicular stomatitis virus) but no pronounced effect on non-enveloped viruses (murine norovirus, rotavirus).

“As there are far more enveloped viruses known than tested in this study, further investigations are necessary,” Dr. Steinmann said.

“Human breast milk efficiently inactivates HCV in vitro and neither the Centers for Disease Control nor the American Association for the Study of Liver Diseases argues against breastfeeding from HCV infected women unless they have cracked or bleeding nipples,” Dr. Steinmann concluded.

Dr. Jhaveri’s editorial concludes, “After reading this article, when we clinicians next encounter an HCV infected patient that just delivered a healthy infant and wants to breastfeed, we have yet another reason to say ‘Breast is Best.'”

Intensive insulin for type 2 diabetes: the risk of causing harm.

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The ACCORD study showed that aggressive intensification of glycaemic control in patients with type 2 diabetes can increase mortality (hazard ratio [HR] 1·22, 95% CI 1·01—1·46), including death from cardiovascular causes (1·35, 1·04—1·76).1 The reason for this unexpected finding is unknown. Of note was the high percentage of intensively treated patients receiving insulin therapy (77%) or thiazolidinedione therapy (with or without insulin) (92%), and their greater weight gain (3·5 kg vs 0·4 kg).1 Results of post-hoc analyses did not support the hypothesis that increased hypoglycaemia in patients who were intensively treated caused the excess deaths.2 The analyses showed, however, that a higher baseline HbA1c and a failure to improve average HbA1c throughout the study were linked to the increased mortality.3

In view of the findings of the ACCORD study, we propose that development of insulin resistance in crucial tissues such as the heart is a protective response to persistently raised glucose concentrations. We postulate that overriding insulin resistance in attempts to lower glucose with exogenous insulin—particularly in overweight and obese patients with the most refractory hyperglycaemia—could undo this protection and cause harm.

For decades the dogma has been that insulin resistance is mostly pathological. However, regulation of insulin sensitivity is an integral component of normal metabolic physiology, including, at times, the induction of insulin resistance. For example, in response to even short-term overfeeding, skeletal and cardiac muscle develops insulin resistance,4 which promotes diversion of excess nutrients to adipose tissue for safe storage. We, and others, have proposed that this induction of insulin resistance protects important tissues from nutrient-induced dysfunction.5

The myocardium, with its high energy needs, adapts to the predominant nutrient source, which is free fatty acids (FFA) during fasting and glucose in the fed state. In poorly controlled type 2 diabetes, the reciprocal relationship between FFA and glucose is lost and both are simultaneously raised. This places the myocardium at increased risk of nutrient overload and myocardial glucolipotoxicity.5, 6 We propose, however, that insulin resistance is a safeguard against glucolipotoxicity because it limits myocardial glucose uptake. Treatment of patients with the most refractory hyperglycaemic and hyperlipidaemic type 2 diabetes with large amounts of exogenous insulin could override this block against glucose entry, providing all the ingredients for glucolipotoxicity,6 a process that we have termed insulin-mediated metabolic stress. In the heart, this process would cause a metabolic cardiomyopathy. Jagasia and colleagues7 provided evidence that insulin resistance is easier to override in the myocardium than in skeletal muscle in patients with type 2 diabetes. Exogenous insulin tripled myocardial glucose uptake without compensatory reduction in FFA uptake,7 which is consistent with the capacity of exogenous insulin to drive excess nutrients into the heart. If the same mechanisms of insulin-mediated metabolic stress can function in skeletal muscle, inappropriate high-dose insulin use in patients with type 2 diabetes could also induce a metabolic myopathy that impairs the patient’s ability to exercise.

If our proposition is correct—that intensive treatment of type 2 diabetes with insulin is potentially harmful to overweight and obese patients with the most refractory hyperglycaemia—there should be support for it in clinical trials. In the major trials of intensive versus conventional glucose control, and insulin versus other glucose-lowering therapies, whenever high use of insulin was associated with weight gain of greater than 1 kg per year (ACCORD,1 VADT,8 DIGAMI-29), cardiovascular or all-cause mortality, or both, were increased, reaching statistical significance only in the higher powered ACCORD study. UKPDS, ADVANCE, and ORIGIN did not show increased cardiovascular disease or mortality in the intensive control or insulin therapy groups. However, the patient characteristics and the aggressiveness of insulin use differed greatly from those in ACCORD. Careful analysis showed that UKPDS, ADVANCE, and ORIGIN were not studies of intensive insulin use in obese patients with the most refractory hyperglycaemia. While results of population-based studies have shown increased risk of mortality in patients with type 2 diabetes treated with insulin, they are observational and should be interpreted with caution.10

Patients with type 2 diabetes should be considered individually, because their relative need for insulin resistance as a protective mechanism and the potential for long-term benefit from tight blood glucose control will differ. For example, an overweight individual with type 2 diabetes unable to exercise because of comorbidities will have much more difficulty achieving lifestyle change to overcome a state of positive energy balance (figure). In these patients, insulin resistance might be necessary to protect crucial tissues such as the heart and skeletal muscle against excess nutrient entry. An aggressive approach to lower blood glucose with insulin will override this protection, increasing the risk of insulin-mediated metabolic stress in these key tissues (figure). Furthermore, these patients are least likely to be able to adequately achieve lower HbA1c concentrations—the group that was at highest risk in ACCORD.3 Careful amelioration of very high blood glucose, however, will be necessary in these individuals. At the other end of the spectrum, a patient with type 2 diabetes who can avoid positive energy balance by lifestyle change will be at much lower risk of the harmful consequences of an aggressive approach to glucose lowering with insulin.

The safety of insulin sensitisers is probably associated with the mechanism by which they work. Those that enhance nutrient detoxification should be beneficial. Such agents are very different from insulin in that they reduce and do not override insulin resistance. Metformin and thiazolidinedione drugs both have mechanisms of action that include nutrient detoxification.5 The development of new insulin sensitisers that do not have a nutrient detoxification mechanism might not be advisable.

Further studies of the effect of insulin therapy on myocardial and skeletal muscle nutrient uptake, storage, and function in obese patients with type 2 diabetes are necessary to further explore the concept of insulin-mediated metabolic stress. Ultimately, carefully designed randomised clinical trials with long-term outcome data will be necessary to assess the safety of insulin therapy, and how best to use it, in obese patients with type 2 diabetes who do not achieve acceptable glycaemic control by other therapies. The results of the ACCORD study suggest that the combination of insulin with thiazolidinedione agents should be used with considerable caution.1 The use of insulin in combination with newer agents that avert positive energy balance, such as the glucagon-like peptide 1 mimetics, warrants particular attention in this challenging group of patients.

CJN has received speaking fees from AstraZeneca, Eli Lilly, GlaxoSmithKline, Merck Sharp and Dhome, Novartis, and Novo Nordisk; and has been a member of an advisory board for Sanofi Aventis. NBR and MP declare that they have no conflicts of interest.

References

1 Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med 2008;358: 2545-2559. CrossRef | PubMed

2 Bonds DE, Miller ME, Bergenstal RM, et al. The association between symptomatic, severe hypoglycaemia and mortality in type 2 diabetes: retrospective epidemiological analysis of the ACCORD study. BMJ 2010; 340: b4909. CrossRef | PubMed

3 Riddle MC, Ambrosius WT, Brillon DJ, et al. Epidemiologic relationships between A1C and all-cause mortality during a median 3·4-year follow-up of glycemic treatment in the ACCORD trial. Diabetes Care 2010; 33: 983-990. CrossRef | PubMed

4 Kraegen EW, Saha AK, Preston E, et al. Increased malonyl-CoA and diacylglycerol content and reduced AMPK activity accompany insulin resistance induced by glucose infusion in muscle and liver of rats. Am J Physiol Endocrinol Metab 2006;290: E471-E479. CrossRef | PubMed

5 Nolan CJ, Damm P, Prentki M. Type 2 diabetes across generations: from pathophysiology to prevention and management.Lancet 2011; 378: 169-181. Summary | Full Text | PDF(856KB) | CrossRef | PubMed

6 Taegtmeyer H, Stanley WC. Too much or not enough of a good thing? Cardiac glucolipotoxicity versus lipoprotection. J Mol Cell Cardiol 2010; 50: 2-5. CrossRef | PubMed

7 Jagasia D, Whiting JM, Concato J, Pfau S, McNulty PH. Effect of non-insulin-dependent diabetes mellitus on myocardial insulin responsiveness in patients with ischemic heart disease. Circulation 2001; 103: 1734-1739. CrossRef | PubMed

8 Duckworth W, Abraira C, Moritz T, et al. Glucose control and vascular complications in veterans with type 2 diabetes. N Engl J Med 2009; 360: 129-139. CrossRef | PubMed

9 Mellbin LG, Malmberg K, Norhammar A, Wedel H, Ryden L. Prognostic implications of glucose-lowering treatment in patients with acute myocardial infarction and diabetes: experiences from an extended follow-up of the Diabetes Mellitus Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) 2 Study. Diabetologia 2011; 54: 1308-1317. CrossRef |PubMed

10 Currie CJ, Poole CD, Evans M, Peters JR, Morgan CL. Mortality and other important diabetes-related outcomes with insulin vs other antihyperglycemic therapies in Type 2 Diabetes. J Clin Endocrinol Metab 2013; 98: 668-677. CrossRef | PubMed

Source: Lancet

Intensive insulin for type 2 diabetes: the risk of causing harm.

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The ACCORD study showed that aggressive intensification of glycaemic control in patients with type 2 diabetes can increase mortality (hazard ratio [HR] 1·22, 95% CI 1·01—1·46), including death from cardiovascular causes (1·35, 1·04—1·76).1 The reason for this unexpected finding is unknown. Of note was the high percentage of intensively treated patients receiving insulin therapy (77%) or thiazolidinedione therapy (with or without insulin) (92%), and their greater weight gain (3·5 kg vs0·4 kg).1 Results of post-hoc analyses did not support the hypothesis that increased hypoglycaemia in patients who were intensively treated caused the excess deaths.2 The analyses showed, however, that a higher baseline HbA1c and a failure to improve average HbA1c throughout the study were linked to the increased mortality.3

In view of the findings of the ACCORD study, we propose that development of insulin resistance in crucial tissues such as the heart is a protective response to persistently raised glucose concentrations. We postulate that overriding insulin resistance in attempts to lower glucose with exogenous insulin—particularly in overweight and obese patients with the most refractory hyperglycaemia—could undo this protection and cause harm.

For decades the dogma has been that insulin resistance is mostly pathological. However, regulation of insulin sensitivity is an integral component of normal metabolic physiology, including, at times, the induction of insulin resistance. For example, in response to even short-term overfeeding, skeletal and cardiac muscle develops insulin resistance,4 which promotes diversion of excess nutrients to adipose tissue for safe storage. We, and others, have proposed that this induction of insulin resistance protects important tissues from nutrient-induced dysfunction.5

The myocardium, with its high energy needs, adapts to the predominant nutrient source, which is free fatty acids (FFA) during fasting and glucose in the fed state. In poorly controlled type 2 diabetes, the reciprocal relationship between FFA and glucose is lost and both are simultaneously raised. This places the myocardium at increased risk of nutrient overload and myocardial glucolipotoxicity.5, 6 We propose, however, that insulin resistance is a safeguard against glucolipotoxicity because it limits myocardial glucose uptake. Treatment of patients with the most refractory hyperglycaemic and hyperlipidaemic type 2 diabetes with large amounts of exogenous insulin could override this block against glucose entry, providing all the ingredients for glucolipotoxicity,6 a process that we have termed insulin-mediated metabolic stress. In the heart, this process would cause a metabolic cardiomyopathy. Jagasia and colleagues7 provided evidence that insulin resistance is easier to override in the myocardium than in skeletal muscle in patients with type 2 diabetes. Exogenous insulin tripled myocardial glucose uptake without compensatory reduction in FFA uptake,7 which is consistent with the capacity of exogenous insulin to drive excess nutrients into the heart. If the same mechanisms of insulin-mediated metabolic stress can function in skeletal muscle, inappropriate high-dose insulin use in patients with type 2 diabetes could also induce a metabolic myopathy that impairs the patient’s ability to exercise.

If our proposition is correct—that intensive treatment of type 2 diabetes with insulin is potentially harmful to overweight and obese patients with the most refractory hyperglycaemia—there should be support for it in clinical trials. In the major trials of intensive versus conventional glucose control, and insulin versus other glucose-lowering therapies, whenever high use of insulin was associated with weight gain of greater than 1 kg per year (ACCORD,1 VADT,8 DIGAMI-29), cardiovascular or all-cause mortality, or both, were increased, reaching statistical significance only in the higher powered ACCORD study. UKPDS, ADVANCE, and ORIGIN did not show increased cardiovascular disease or mortality in the intensive control or insulin therapy groups. However, the patient characteristics and the aggressiveness of insulin use differed greatly from those in ACCORD. Careful analysis showed that UKPDS, ADVANCE, and ORIGIN were not studies of intensive insulin use in obese patients with the most refractory hyperglycaemia. While results of population-based studies have shown increased risk of mortality in patients with type 2 diabetes treated with insulin, they are observational and should be interpreted with caution.10

Patients with type 2 diabetes should be considered individually, because their relative need for insulin resistance as a protective mechanism and the potential for long-term benefit from tight blood glucose control will differ. For example, an overweight individual with type 2 diabetes unable to exercise because of comorbidities will have much more difficulty achieving lifestyle change to overcome a state of positive energy balance (figure). In these patients, insulin resistance might be necessary to protect crucial tissues such as the heart and skeletal muscle against excess nutrient entry. An aggressive approach to lower blood glucose with insulin will override this protection, increasing the risk of insulin-mediated metabolic stress in these key tissues (figure). Furthermore, these patients are least likely to be able to adequately achieve lower HbA1cconcentrations—the group that was at highest risk in ACCORD.3 Careful amelioration of very high blood glucose, however, will be necessary in these individuals. At the other end of the spectrum, a patient with type 2 diabetes who can avoid positive energy balance by lifestyle change will be at much lower risk of the harmful consequences of an aggressive approach to glucose lowering with insulin.

The safety of insulin sensitisers is probably associated with the mechanism by which they work. Those that enhance nutrient detoxification should be beneficial. Such agents are very different from insulin in that they reduce and do not override insulin resistance. Metformin and thiazolidinedione drugs both have mechanisms of action that include nutrient detoxification.5 The development of new insulin sensitisers that do not have a nutrient detoxification mechanism might not be advisable.

Further studies of the effect of insulin therapy on myocardial and skeletal muscle nutrient uptake, storage, and function in obese patients with type 2 diabetes are necessary to further explore the concept of insulin-mediated metabolic stress. Ultimately, carefully designed randomised clinical trials with long-term outcome data will be necessary to assess the safety of insulin therapy, and how best to use it, in obese patients with type 2 diabetes who do not achieve acceptable glycaemic control by other therapies. The results of the ACCORD study suggest that the combination of insulin with thiazolidinedione agents should be used with considerable caution.1 The use of insulin in combination with newer agents that avert positive energy balance, such as the glucagon-like peptide 1 mimetics, warrants particular attention in this challenging group of patients.

Source: Lancet

 

Synthesis of customized petroleum-replica fuel molecules by targeted modification of free fatty acid pools in Escherichia coli.

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Abstract

Biofuels are the most immediate, practical solution for mitigating dependence on fossil hydrocarbons, but current biofuels (alcohols and biodiesels) require significant downstream processing and are not fully compatible with modern, mass-market internal combustion engines. Rather, the ideal biofuels are structurally and chemically identical to the fossil fuels they seek to replace (i.e., aliphatic n– and iso–alkanes and -alkenes of various chain lengths). Here we report on production of such petroleum-replica hydrocarbons inEscherichia coli. The activity of the fatty acid (FA) reductase complex from Photorhabdus luminescens was coupled with aldehyde decarbonylase from Nostoc punctiforme to use free FAs as substrates for alkane biosynthesis. This combination of genes enabled rational alterations to hydrocarbon chain length (Cn) and the production of branched alkanes through upstream genetic and exogenous manipulations of the FA pool. Genetic components for targeted manipulation of the FA pool included expression of a thioesterase fromCinnamomum camphora (camphor) to alter alkane Cn and expression of the branched-chain α-keto acid dehydrogenase complex and β-keto acyl-acyl carrier protein synthase III from Bacillus subtilis to synthesize branched (iso-) alkanes. Rather than simply reconstituting existing metabolic routes to alkane production found in nature, these results demonstrate the ability to design and implement artificial molecular pathways for the production of renewable, industrially relevant fuel molecules.

 

Source: pnas.org

Eating oily fish ‘can extend life’.

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fish

Eating oily fish rich in omega-3 fatty acids can add years to your life, a study has shown.

Higher blood levels of omega-3 reduce the chances of dying from heart disease by more than a third, according to the research.

They cut the overall risk of dying by as much as 27 per cent.

Scientists found that people with the largest amounts of the fatty acids in their blood lived on average 2.2 years longer than those with lower levels.

“Although eating fish has long been considered part of a healthy diet, few studies have assessed blood omega-3 levels and total deaths in older adults,” said lead researcher Dr Dariush Mozaffarian, from the Harvard School of Public Health in the US.

“Our findings support the importance of adequate blood omega-3 levels for cardiovascular health, and suggest that later in life these benefits could actually extend the years of remaining life.”

The scientists analysed 16 years of data from around 2,700 US adults aged 65 and older taking part in the Cardiovascular Health Study (CHS).

Participants gave blood samples and were questioned about their health, medical history and lifestyle.

Three key omega-3 fatty acids, both separately and together, were associated with a significantly reduced risk of death.

One, docosahexaenoic acid ( DHA) , was linked to a 40% lower risk of death due to coronary heart disease. This was especially true for deaths caused by heart rhythm disturbances.

Another omega-3 compound, docosapentaenoic acid (DPA) was strongly associated with a lower risk of death from stroke.

The third type of omega-3, eicosapentaenoic acid (EPA) was linked to a reduced risk of non-fatal heart attack.

Overall, participants with the highest levels of all three types of fatty acid had a 27 per cent lower risk of death from all causes.

The findings appear in the online edition of the journal Annals of Internal Medicine.

Oily fish, such as mackerel, tuna and sardines, is the most important source of omega-3. The fatty acids can also be found in flaxseed, walnuts and rapeseed oil.

Source: .independent.co.uk

‘Fat’ drug could treat epilepsy.

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A substance made by the body when it uses fat as fuel could provide a new way of treating epilepsy, experts hope.

Researchers in London who have been carrying out preliminary tests of the fatty acid treatment, report their findings in Neuropharmacology journal.

They came up with the idea because of a special diet used by some children with severe, drug resistant epilepsy to help manage their condition.

The ketogenic diet is high in fat and low in carbohydrate.

The high fat, low carbohydrate diet is thought to mimic aspects of starvation by forcing the body to burn fats rather than carbohydrates.

 “Start Quote

The identification of these fatty acids is an exciting breakthrough”

Simon WigglesworthEpilepsy Action

Although often effective, the diet has attracted criticism, as side-effects can be significant and potentially lead to constipation, hypoglycaemia, retarded growth and bone fractures.

By pinpointing fatty acids in the ketogenic diet that are effective in controlling epilepsy, researchers hope they can develop a pill for children and adults that could provide similar epilepsy control without the side-effects.

In early trials, the scientists, from Royal Holloway and University College London, say they have identified fatty acids that look like good candidates for the job.

They found that not only did some of the fatty acids outperform a regular epilepsy medication called valproate in controlling seizures in animals, they also had fewer side-effects.

But many more tests are needed to determine if the treatment would be safe and effective in humans.

Prof Matthew Walker, from the Institute of Neurology, University College London, said: “Epilepsy affects over 50 million people worldwide and approximately a third of these people have epilepsy that is not adequately controlled by our present treatments.

“This discovery offers a whole new approach to the treatment of drug-resistant epilepsies in children and adults.”

Simon Wigglesworth, deputy chief executive at Epilepsy Action, said: “We know the ketogenic diet can be a highly effective treatment for children with difficult to control epilepsy and it is starting to be used for adults.

“The diet is high in fats and low in carbohydrates and the balance of the diet needs to be carefully worked out for each child. Although some children manage the diet very well, others find the diet unpleasant and difficult to follow. Children can also experience side-effects including constipation and weight loss.

“The identification of these fatty acids is an exciting breakthrough. The research means that children and adults with epilepsy could potentially benefit from the science behind the ketogenic diet without dramatically altering their eating habits or experiencing unpleasant side-effects.

“We look forward to seeing how this research progresses.”

Source:BBC

Which Oil Will Help You Absorb Nutrients Better?

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You’re probably aware that in order to absorb all of the extremely healthy fat-soluble nutrients in your food, compounds like lutein, beta-carotene and vitamin E, for instance, you’ve got to eat them with some fat.

So perhaps you always add olive oil to your salads or eat your veggies with butter to absorb all of those valuable nutrients.

This is a smart health move, but did you know that not all oils are created equal when it comes to nutrient absorption? Some work better than others and can actually enhance the amount of nutrients your body receives from the food you eat.

Coconut Oil is Superior in Enhancing Nutrient Absorption

A new animal study compared the effects of feeding coconut oil (a saturated fat) versus safflower oil (a polyunsaturated fat) on the absorption of carotenoids from tomatoes. Coconut oil enhanced tissue uptake of tomato carotenoids to a greater degree than safflower oil, a benefit the researchers suggested may be due to coconut oil’s medium chain fatty acids (MCFAs):1

“These results may have been due to the large proportion of medium chain fatty acids in coconut oil, which might have caused a shift in cholesterol flux to favor extrahepatic carotenoid tissue deposition.”

Coconut oil is nature’s richest source of healthy MCFAs. By contrast, most common vegetable or seed oils are comprised of long chain fatty acids (LCFAs). There are several reasons why these long-chain fatty acids are not as healthy for you as the MCFAs in coconut oil.

Why Choose an Oil Like Coconut Oil?

In addition to its ability to potentially allow you to absorb more antioxidants and other nutrients from your food, MCFAs are smaller than LCFAs, which means they permeate cell membranes easily, and do not require lipoproteins or special enzymes to be utilized effectively by your body. Further:

  • MCFAs are easily digested, thus putting less strain on your digestive system. This is especially important for those of you with digestive or metabolic concerns.
  • MCFAs are sent directly to your liver, where they are immediately converted into energy rather than being stored as fat.
  • MCFAs in coconut oil can actually help stimulate your body’s metabolism, leading to weight loss.

There are numerous studies showing that MCFAs promote weight loss, including one study that showed rats fed LCFAs stored body fat, while rats fed MCFAs reduced body fat and improved insulin sensitivity and glucose tolerance.2 Yet another study found that overweight men who ate a diet rich in MCFAs lost more fat tissue compared to those eating a high-LCFA diet, presumably due to increased energy expenditure and fat oxidation from the MCFA intake. Researchers concluded:3

“Thus, MCTs may be considered as agents that aid in the prevention of obesity or potentially stimulate weight loss.”

Coconut oil earns even more “points” because it’s rich in lauric acid, which converts in your body to monolaurin – a compound also found in breast milk that strengthens immunity. Caprylic acid, another coconut fatty acid present in smaller amounts, is another antimicrobial component. Plus, using coconut oil as your primary cooking oil is important because it is the only one that is stable enough to resist heat-induced damage. When choosing a coconut oil, make sure you choose an organic coconut oil that is unrefined, unbleached, made without heat processing or chemicals, and does not contain GM ingredients. On the other hand, in the case of LCFA-rich vegetable oils:

  • LCFAs are difficult for your body to break down — they must be packaged with lipoproteins or carrier proteins and require special enzymes for digestion.
  • LCFAs put more strain on your pancreas, your liver and your entire digestive system.
  • LCFAs are predominantly stored in your body as fat.
  • LCFAs, when oxidized, can both injure and deposit within arteries, contributing to both blood vessel inflammation and plaque build-up.

Polyunsaturated fats, which include common vegetable oils such as corn, soy, safflower, sunflower and canola, are absolutely the worst oils to use in cooking. These omega-6 oils are highly susceptible to heat damage because of their multiple double carbon bonds. If you’ve been shunning coconut oil because it’s a saturated fat, you needn’t worry. Saturated fats are actually essential and quite good for you.

Enzymes: Another Tool to Enhance Nutrient Absorption

Enzymes are composed of amino acids and are secreted by your body to help catalyze functions that would normally not occur at physiological temperatures. They literally make magic happen and are absolutely vital to your life.

More than 3,000 different enzymes have been identified, and some experts believe there may be another 50,000 we have yet to discover. Each enzyme has a different function—like 3,000 specialized keys cut to fit 3,000 different locks. In this analogy, the locks are biochemical reactions, which include not only energy production and absorption of oxygen, but getting nutrients into your cells.

Chronic malabsorption can lead to a variety of illnesses. Think about it—if your body doesn’t have the basic nutritional building blocks it needs, your health and ability to recover from illness will be compromised. Enzyme deficiency results in poor digestion and poor nutrient absorption. This creates a variety of gastrointestinal symptoms, including:

  • Constipation
  • Bloating
  • Cramping
  • Flatulence and belching
  • Heartburn and acid reflux

Many people are, unfortunately, lacking in the enzyme department, as diets heavy in cooked, processed, and sugary foods, combined with overuse of pharmaceutical drugs such as antibiotics, deplete your body’s ability to make enzymes. Heating your food above 116 degrees F also renders most enzymes inactive for destroys them. This is one of the reasons it’s so important to eat your foods raw. Raw foods are enzyme-rich, and consuming them decreases your body’s burden to produce its own enzymes. The more food that you can eat raw, the better.

A Healthy Gut Encourages Optimal Nutrient Absorption

Similar to enzymes, your gut flora, the microorganisms living in your intestines, continually and dynamically affect your health. In fact, these beneficial bacteria secrete essential enzymes for us. The Lactobacillus genus of probiotics, for instance, got their name from the fact that they break down lactose (milk sugar) into lactic acid with the enzyme lactase. This, in fact, is one reason why culturing was invented in the first place, as only a limited number of individuals with a particular European genotype are capable of producing the lactase enzyme late into life — most lose the ability soon after weaning from breast milk.

Good bacteria that you take in, either from fermented foods or in supplement form, also prevent the growth of less desirable ones by competing for both nutrition and attachment sites in the tissues of your alimentary canal. These friendly bacteria also aid digestion and nutrient absorption so that you’re able to get more benefit from the foods you eat.

In fact, without good gut bacteria, your body cannot absorb certain undigested starches, fiber, and sugars. The friendly bacteria in your digestive tract convert these carbohydrates into primary sources of important energy. These bacteria also produce a secondary layer of indispensable fermentation byproducts such as bacteriocins (which fight infection), beta glucans (which modulate immunity), and the entire B group vitamin series, to name but only a few of the nutrients they are capable of producing for us. Through this continual process of biotransformation that happens 24-7 in our gut, we are in many ways vitamin- and “medicine”-producing factories!

Eating fermented vegetables, and other fermented foods, like kefir, regularly is one of the best ways to nourish your gut flora for optimal nutrient absorption.

The common thread that you may have noticed here is a traditional, healthy diet. When you eat the foods your body is designed for, foods like coconut oil and other fresh, raw, minimally processed sources of fat, protein and healthy carbs, you will naturally encourage your body to utilize all that it can from the healthy foods you eat. So remember, when you need an oil to add to your meals, choosing coconut oil over polyunsaturated vegetable oils like safflower oil may be a simple way to boost your body’s nutrient intake for optimal health.

Just make sure that when you use coconut oil you are certain, like all your foods, you are getting the highest quality source possible.

Source: Dr. Mercola