Biotin & Triglycerides - why perhaps Fish Oil and Niacin may actually help a little in Autism & Schizophrenia

Far back in this blog, I wrote a post about fish oil.  Omega 3 oils are definitely good for your general health, but do they help with autism?  They are also claimed to help with ADHD and improve your NT child’s cognitive performance.

On critical review of the evidence, it seemed that the benefit was far from conclusive.  There was one very positive study, that neither the authors nor anyone else could repeat.

The following review of the literature by the University of Maryland show that, as with autism, studies on fish oil in depression, ADHD, bipolar and schizophrenia show conflicting results.

Omega-3 fatty acids

Some of the “cognitive enhancing” fish oil products are extremely expensive and I showed that regular fish consumption was far cheaper and likely to be as effective.

There is an issue of just how big an effect you are looking for.  We can all imagine tiny effects, but you really want an effect that everyone else notices.

Monty, aged 11 with ASD, eats lots of fish, mainly because he loves it.  He is not at all put off by those little bones.

The effect of fish oil on Monty was not noticeable.

Biotin

A recent post contained a study from Greece, where they found a remarkably high proportion of kids with ASD with a biotin deficiency.  This had not shown up on the standard test, because the standard test is strangely not for biotin at all; it tests for biotinidase, a related enzyme.

Identifying a biotin deficiency is not easy, blood tests are not helpful and you have to look at certain compounds found in urine.  As a result your local laboratory may not offer a useful test for biotin.

Since supplementation with pharmacological doses of biotin is known to be harmless, the practical way forward is to try it.

In the midst of looking at the relative effect of different primary antioxidants, I was substituting one thiol antioxidant (ALA) for another (NAC) to see if there was any obvious difference.  I could give lots of reasons, with scientific papers to back them up, as to why 0.6g of ALA plus 1.8g of NAC might be “better” than 2.4g of NAC, but it is not.  If anything, it might be worse.

Then I tried Carnosine in combination with NAC and again I could see absolutely no effect.

Then I decided to go back to my original NAC regime and add the biotin that had been on the shelf since Christmas. Very surprisingly, the effect that I thought might show up with ALA, showed up with biotin.  

It was not a huge effect, but a small step forward, that Monty’s assistant at school also noticed.  He was more calm and altogether more "normal". 

Does this mean Monty has a biotin deficiency?  It is of course possible.  In the Greek study 4% of the kids were thought to have such a deficiency, far more than expected, and most did respond, in varying degrees, to biotin supplements.  Unfortunately they only gave the biotin to the 4%; I would like to know what would have happened to the remaining 96%.

Biotin lowers Triglycerides and Elevated Triglycerides are associated with Mood Disorders   

Biotin is a B vitamin, but very little is actually known about it.

Then I found the link I was looking for.

Biotin does not lower cholesterol, but it does reduce (in a big way) your Triglycerides.

Several studies have shown that elevated Triglycerides are associated with all kinds of disorders: bipolar, depression and schizophrenia.  These studies suggested a causal link between the mood disorder and the elevated triglyerides.

Other Effects on Mood

          Besides depression, high levels of triglycerides are also correlated with other affective disorders including bipolar disorder (manic depression), schizoaffective disorders, aggression and hostility. In fact, the poor nutritional status of many depressed persons, who often have diets high in fats, can be improved to lessen the depression, according to Charles Glueck, MD, medical director of the Cholesterol Center of Jewish Hospital in Cincinnati.

"We have shown that in patients with high triglycerides who were in a depressive state, the more you lower the triglycerides, the more you alleviate the depression," Glueck wrote in a 1993 article in Biological Psychiatry.

According to the U.S. Centers for Disease Control and Prevention (CDC), most Americans aren't aware of the role triglycerides play in physical and mental health. A five-year study of more than 5,000 Americans found that 33 percent of them had borderline high triglyceride levels.

Improvement in symptoms of depression and in an index of life stressors accompany treatment of severe hypertriglyceridemia.

In 14 men and nine women referred because of severe primary hypertriglyceridemia, our specific aim in a 54-week single-blind treatment (Rx) period was to determine whether triglyceride (TG) lowering with a Type V diet and Lopid would lead to improvement in symptoms of depression, improvement in an index of life stressors, change in locus of control index, and improved cognition, as serially tested by Beck (BDI), Hassles (HAS) and HAS intensity indices, Locus of Control index, and the Folstein Mini-Mental status exam. On Rx, median TG fell 47%, total cholesterol (TC) fell 15%, and HDLC rose 19% (all p < or = 0.001). BDI fell at all nine Rx visits (p < or = 0.001), a major reduction in a test of depressive symptoms. The HAS score also fell at all nine visits (p < or = 0.05 - < or = 0.001). Comparing pre-Rx baseline BDI vs BDI at 30 and 54 weeks on Rx, there was a major shift towards absence or amelioration of depressive symptoms (chi 2= 5.9, p = 0.016). On Rx, the greater the percent reduction in TG, the greater the percent fall in BDI (r = 0.47, p < or = 0.05); the greater the percent reduction in TC, the greater the percent fall in HAS (r = 0.41, p < or = 0.05). Improvement in the BDI and HAS accompanied treatment of severe hypertriglyceridemia, possibly by virtue of improved cerebral perfusion and oxygenation. There may be a reversible causal relationship between high TG and symptoms of depression.

Mood symptoms and serum lipids in acute phase of bipolar disorder inTaiwan.

 

Abstract

Serum lipids have been found to play important roles in the pathophysiology of mood disorders. The aim of the present study was therefore to investigate the relationship between symptom dimensions and serum cholesterol and triglyceride levels, and to explore correlates of lipid levels during acute mood episodes of bipolar I disorder in Taiwan. Measurements were taken of the serum cholesterol and triglyceride levels in patients with bipolar I disorder hospitalized for acute mood episodes (68 manic, eight depressive, and six mixed). The relationships between serum lipids levels and various clinical variables were examined. The mean serum levels of cholesterol (4.54 mmol/L) and triglycerides (1.16 mmol/L) of sampled patients were comparable to those of the general population in the same age segment. Severe depressive symptoms and comorbid atopic diseases were associated with higher serum cholesterol levels. A negative association was noted between serum triglyceride levels and overall psychiatric symptoms. Compared with previous studies on Western populations, racial differences may exist in lipids profiles of bipolar disorder patients during acute mood episodes. Increased serum cholesterol levels may have greater relevance to immunomodulatory system and depressive symptoms, in comparison with manic symptoms.

Biotin supplementation reduces plasma triacylglycerol and VLDL in type 2 diabetic patients and in non-diabetic subjects with hypertriglyceridemia.

Abstract

Biotin is a water-soluble vitamin that acts as a prosthetic group of carboxylases. Besides its role as carboxylase prosthetic group, biotin regulates gene expression and has a wide repertoire of effects on systemic processes. The vitamin regulates genes that are critical in the regulation of intermediary metabolism. Several studies have reported a relationship between biotin and blood lipids. In the present work we investigated the effect of biotin administration on the concentration of plasma lipids, as well as glucose and insulin in type 2 diabetic and nondiabetic subjects. Eighteen diabetic and 15 nondiabetic subjects aged 30-65 were randomized into two groups and received either 61.4 micromol/day of biotin or placebo for 28 days. Plasma samples obtained at baseline and after treatment were analyzed for total triglyceride, cholesterol, very low density lipoprotein (VLDL), glucose and insulin. We found that the vitamin significantly reduced (P=0.005) plasma triacylglycerol and VLDL concentrations. Biotin produced the following changes (mean of absolute differences between 0 and 28 day treatment+/-S.E.M.): a) triacylglycerol -0.55+/-0.2 in the diabetic group and -0.92+/-0.36 in the nondiabetic group; b) VLDL: -0.11+/-0.04 in the diabetic group and -0.18+/-0.07 in the nondiabetic group. Biotin treatment had no significant effects on cholesterol, glucose and insulin in either the diabetic or nondiabetic subjects. We conclude that pharmacological doses of biotin decrease hypertriglyceridemia. The triglyceride-lowering effect of biotin suggests that biotin could be used in the treatment of hypertriglyceridemia.

The hypotriglyceridemic effect of biotin supplementation involves increased levels of cGMP and AMPK activation

Abstract

In addition to its role as a carboxylase cofactor, biotin modifies gene expression and has manifold effects on systemic processes. Several studies have shown that biotin supplementation reduces hypertriglyceridemia. We have previously reported that this effect is related to decreased expression of lipogenic genes. In the present work, we analyzed signaling pathways and posttranscriptional mechanisms involved in the hypotriglyceridemic effects of biotin. Male BALB/cAnN Hsd mice were fed a control or a biotin-supplemented diet (1.76 or 97.7 mg of free biotin/kg diet, respectively for 8 weeks after weaning. The abundance of mature sterol regulatory element-binding protein (SREBP-1c), fatty-acid synthase (FAS), total acetyl-CoA carboxylase-1 (ACC-1) and its phosphorylated form, and AMP-activated protein kinase (AMPK) were evaluated in the liver. We also determined the serum triglyceride concentrations and the hepatic levels of triglycerides and cyclic GMP (cGMP). Compared to the control group, biotin-supplemented mice had lower serum and hepatic triglyceride concentrations. Biotin supplementation increased the levels of cGMP and the phosphorylated forms of AMPK and ACC-1 and decreased the abundance of the mature form of SREBP-1c and FAS. These data provide evidence that the mechanisms by which biotin supplementation reduces lipogenesis involve increased cGMP content and AMPK activation. In turn, these changes lead to augmented ACC-1 phosphorylation and decreased expression of both the mature form of SREBP-1c and FAS. Our results demonstrate for the first time that AMPK is involved in the effects of biotin supplementation and offer new insights into the mechanisms of biotin-mediated hypotriglyceridemic effects.

Triglycerides are also elevated in autism:-

Alterations in lipid profile of autistic boys: a case control study.

Abstract

We hypothesize that autism is associated with alterations in the plasma lipid profile and that some lipid fractions in autistic boys may be significantly different than those of healthy boys. A matched case control study was conducted with 29 autistic boys (mean age, 10.1 +/- 1.3 years) recruited from a school for disabled children and 29 comparable healthy boys from a neighboring elementary school in South Korea. Fasting plasma total cholesterol (T-Chol), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), the LDL/HDL ratio, and 1-day food intakes were measured. Multiple regression analyses were performed to assess the association between autism and various lipid fractions. The mean TG level (102.4 +/- 52.4 vs 70.6 +/- 36.3; P = .01) was significantly higher, whereas the mean HDL-C level (48.8 +/- 11.9 vs 60.5 +/- 10.9 mg/dL; P = .003) was significantly lower in cases as compared to controls. There was no significant difference in T-Chol and LDL-C levels between cases and controls. The LDL/HDL ratio was significantly higher in cases as compared to controls. Multiple regression analyses indicated that autism was significantly associated with plasma TG (beta = 31.7 +/- 11.9; P = .01), HDL (beta = -11.6 +/- 2.1; P = .0003), and the LDL/HDL ratio (beta = 0.40 +/- 0.18; P = .04). There was a significant interaction between autism and TG level in relation to plasma HDL level (P = .02). Fifty-three percent of variation in the plasma HDL was explained by autism, plasma TG, LDL/HDL ratio, and the interaction between autism and plasma TG level. These results indicate the presence of dyslipidemia in boys with autism and suggest a possibility that dyslipidemia might be a marker of association between lipid metabolism and autism.

Omega-3 Oil and Niacin in Schizophrenia

Like Autism, Schizophrenia is another observational diagnosis, with many different underlying genetic and environmental causes.  I keep referring to it as adult-onset autism.  It is also characterized by oxidative stress.

I found it interesting that two very widely used therapies for schizophrenia are omega-3 fish oil and high doses of niacin.  2 g a day of NAC is another common therapy in schizophrenia.

The clinical trials of omega-3 oil in schizophrenia, are just like the ones in autism, far from conclusive.  Yet people with schizophrenia continue to buy the expensive EPA fish oils, just like many parents of children with autism.

Another very popular treatment is Niacin.

Niacin does many things but these include increasing your HDL (good) cholesterol, reduce LDL (bad) cholesterol and, importantly, can reduce triglycerides by up to 50%.

Management of Hypertriglyceridemia

Niacin in Anxiety

Supplemental Niacinamide Mitigates Anxiety Symptoms: Three Case Reports

Niacin in autism

People do use high dose niacin and niacinamide in autism, but in general niacin levels are totally normal in people with autism, according to this study:-

Nutritional and metabolic status of children with autism vs. neurotypical children, and the association with autism severity

For the vitamins, the only significant difference was a 20% lower biotin (p < 0.001) in the children with autism. There were possibly significant (p < 0.05) lower levels of vitamin B5, vitamin E, and total carotenoids. Vitamin C was possibly slightly higher in the children with autism. Vitamin B6 (measured as the active form, P5P, in the RBC) had an unusually broad distribution in children with autism compared to controls (see Figure ​Figure1),1), with the levels in the children with autism having 3 times the standard deviation of the neurotypical children.

Niacin was very similar in the autism group (7.00 μg/l and the control group (7.07 μg/l)

Other interesting findings highlighted the usual metabolic differences:-

·        ATP, NADH, and NAHPH were significantly different between the autism and neurotypical groups

·        Sulfation, methylation, glutathione, and oxidative stress biomarkers which were significantly different between the autism and neurotypical groups

·        Amino Acids which were significantly different between the autism and neurotypical groups, rescaled to the average neurotypical value

Peter Triglyceride Hypothesis in Autism & Schizophrenia

Elevated triglycerides in autism/schizophrenia may contribute to behavioral/mood problems.  The lipid contribution to the dysfunction may be correlated to elevation of triglycerides.  In other words triglycerides aggravate the existing disorder.

Some CAM treatments currently used in autism/schizophrenia, including high dose niacin, high dose biotin and high dose omega 3 oils may be effective due to their ability to lower triglycerides.

Biotin may be the safest, cheapest and most effective option to reduce triglycerides and improve mood/behavior.

The underlying cause of lipid dysfunction in autism/schizophrenia is the ongoing oxidative stress.

Fish oil is claimed to be good for your heart, but it has been shown not to affect cholesterol levels.  In some studies it did lower triglycerides.  In some countries doctors prescribe omega-3 oil to patients with stubbornly high triglycerides.  Perhaps they should read the research and try biotin?

  

Other functions of biotin

Biotin does have other more complex functions and the triglycerides may, so to speak, be a red herring.

Regulation of gene expression by biotin (review).

Abstract

In mammals, biotin serves as coenzyme for four carboxylases, which play essential roles in the metabolism of glucose, amino acids, and fatty acids. Biotin deficiency causes decreased rates of cell proliferation, impaired immune function, and abnormal fetal development. Evidence is accumulating that biotin also plays an important role in regulating gene expression, mediating some of the effects of biotin in cell biology and fetal development. DNA microarray studies and other gene expression studies have suggested that biotin affects transcription of genes encoding cytokines and their receptors, oncogenes, genes involved in glucose metabolism, and genes that play a role in cellular biotin homeostasis. In addition, evidence has been provided that biotin affects expression of the asialoglycoprotein receptor and propionyl-CoA carboxylase at the post-transcriptional level. Various pathways have been identified by which biotin might affect gene expression: activation of soluble guanylate cyclase by biotinyl-AMP, nuclear translocation of NF-kappaB (in response to biotin deficiency), and remodeling of chromatin by biotinylation of histones. Some biotin metabolites that cannot serve as coenzymes for carboxylases can mimic biotin with regard to its effects on gene expression. This observation suggests that biotin metabolites that have been considered "metabolic waste" in previous studies might have biotin-like activities. These new insights into biotin-dependent gene expression are likely to lead to a better understanding of roles for biotin in cell biology and fetal development.

It does appear that biotin is more important than generally appreciated. 

Conclusion

In earlier posts I highlighted that elevated cholesterol is a bio-marker for inflammation.  In a large sub-group in autism, cholesterol is elevated.

In today’s post we looked at  a different type of lipid, triglycerides, they have a different role to cholesterol.  Not surprisingly the lipid profile is dysfunction, since it is closely linked to oxidative stress, which appears to be at the root of many problems in autism.

It is extremely easy and inexpensive to check your lipid profile (LDL, HDL and triglycerides); if elevated, there are safe established ways to bring things back to “normal”.

Parents seeing a small positive effect with their fish oil supplements might consider saving a lot of money and seeing if an extremely inexpensive biotin (5mg) supplement has an equal or greater effect.  The cost of biotin would be $2 a month.  The cost of fish oil with anything like the concentration used in the more effective trials (0.84g EPA and 0.7g DHA) will cost around $50 a month and may not lower triglycerides by as much as the cheap biotin.

By measuring the lipid profile before and after, you will be able to determine for yourself the relative merits.

Niacin also has been shown to improve mood/anxiety.  It is used by people with autism and schizophrenia.  Niacin is also extremely effective at reducing triglycerides.  High doses of Niacin can be accompanied by side effects and so use is discouraged.

Biotin levels do seem to be slightly low in autism.  Effective methods of accurately diagnosing deficiency are disputed.  Biotin is very effective at reducing triglycerides.

Elevated triglycerides have been associated with mood disorders and depression.

It seems plausible that the benefits from Omega-3 , niacin and biotin stem from their effectiveness in reducing triglycerides.

Biotin would seem to be a very cost effective and safe way to achieve this, without the side effects of niacin.  

Biotin also appears to have other key functions, including transcription of cytokine genes. Over expression of pro-inflammatory cytokines is a common feature of autism.

NICE Brits 281 and Californian Quacks 305?

I have to thank Paul Whitely  for a post on his website that I am hijacking today.  Click on Paul’s name to go to his blog.

National Institute for Health & Care Excellence (NICE)

NICE is an organisation in the UK, funded by the Department of Health.  They produce excellent guidelines on  most medical conditions for both doctors and patients.  They are all available free on line.

NICE & Autism

NICE are producing a guideline called:-  

Autism, The management and support of children and young people on the autism spectrum.  The guideline is still in the draft stage, but there are two versions:-

Full version (790 pages) 
Summary (40 pages)

You may wonder who on earth is going to read a 790 page document.  The 40 page document does not say a lot, you could summarize it as folows:-

•  Carers (parents) are unsupported, miserable and financially strained

• Children should have access to care and therapy, that does not currently exist

• Local autism teams should have the skills to provide, or organize, the interventions and care recommended in this guideline, but they currently do not have these skills.

• No magic cure exists

 

The NICE list of Dos and Don’ts  (Mainly Don’ts)

DO NOT:-

Do not use the following interventions for the management of core features of autism in children and young people: 

·         antipsychotics

·         antidepressants

·         anticonvulsants

·         exclusion diets (such as gluten- or casein-free diets)  -  sorry Paul

Do not use omega-3 fatty acids to manage sleep problems in children and young people with autism.

Do not use auditory integration training

Do not use the following interventions for children and young people with autism in any context:  

·         secretin

·         chelation

·         hyperbaric oxygen therapy 

DO:-

Consider a social-communication intervention for the management of the core features of autism in children and young people. For pre-school children consider delivering the intervention with parent, carer or teacher mediation. For school-aged children consider delivering the intervention with peer mediation.

Consider the following for children and young people with autism and anxiety who have the verbal and cognitive ability to engage in a cognitive behavioural therapy (CBT) intervention:  

·         group CBT adjusted to the needs of children and young people with autism

·         individual CBT for children and young people who find group-based activities difficult.  

For behavior that challenges, try antipsychotic medication.

  

The 790 page version  -   NICE Brits 281 and Californian Quacks 305

I was rather disappointed by the 40 page version of NICE, so I opened up the 790 page version.  I recommend you do too.  It is totally different.  Some people have spent many 1000’s of hours analysing all the scientific literature on a wide range of biological, social, psychological and educational aspects of autism.

The problem was on page 281.  This is the page where those clever guys over at Stanford 94305, get their research into Glutathione (GSH) mentioned. (94305 is their zip code) 

Then on pages 389/390 NICE give their verdict on the Stanford guys' findings.  They conclude that while NAC does nothing bad, it also did nothing good.

 

Now, I am no medical genius, but nor am I a complete moron. I read the full Stanford research paper as a highly sceptical, but informed, parent. I concluded, as did the Stanford team, that they had found something very important. To get the full report you have to pay $31.50 but I figured it was well worth it. So if this excellent research just gets sliced and diced, and then trashed, in this 790 page review, how much faith do I have in the other 787 pages?

I am with those Quacky Californians on this one.  Those NICE Brits can call me a quack too.

Eat Fish! - all about Omega-3

I did put one very well-known therapy on my list to investigate; that of omega-3 fish oil supplementation.  This is the territory of Complementary and Alternative Medicine (CAM) and maybe not surprisingly there is a lack of high quality research.  This is a pity, because there are some very good scientific reasons why it just might work.

There is only one study that was carried out like a serious clinical drug trial and seemed to show a serious positive result.  It was carried out at the Medical University of Vienna and involved 1.5 g per day of EPA/DHA (0.84g EPA and 0.7g DHA).

It seems nobody else has been able to repeat this result with a similar randomized controlled trial.  What does that tell you?  Maybe those Austrians have a special kind of fish oil ?  Or maybe there is a chemical reaction going on with all that Apple Strudel they were eating?

Even this study did not convince the serious scientists at the University of California, San Francisco.  They did a review of all omega 3 trials from 1966 to September 2008, mentioning autism and omega-3.  It is very readable and their full report  Omega-3 Fatty Acids for Autistic Spectrum Disorder: A Systematic Review  is available free (just click it). A summary, in table form, is on page 1148.  But if you are in a hurry, their conclusion was:-

“there is currently insufficient scientific evidence to determine if omega-3 fatty acids are safe or effective for ASD”

I still have not finished my research, but I can already say with 90% certainly, I know what my final conclusion is likely to be;  Eat Fish ! and I have already implemented it.
 
Here are some undisputed facts:-

1.    Autistic children have lower levels of omega 3 relative to omega 6 and lower levels of the good cholesterol HDL, than typical children.  This implies a lipid metabolism disorder.  If you read my Glutathione (GSH) Part II you will know that such a  lipid disorder should be expected in people with a GSH Redox problem.  NADP/NADPH which is required for lipid and cholesterol synthesis is also required for the GSH Redox chemical reaction.  So if there is a GSH Redox problem (proved already by serious scientists),  NADP/NADPH are highly likely to be involved and if they are, then it is no surprise if omega 3 and cholesterol levels are way off where they should be.  We are already getting side-tracked into the details, just to tell you that NADP is Nicotinamide Adenine Dinucleotide Phosphate and NADPH is the reduced form of the same chemical.  For more info click here.

2.    Omega-3 is proven to be good for the heart, in just about everyone.  The main benefits are related to cholesterol (Hypertriglyceridemia to be precise), cardiovascular disease prevention and high blood pressure.  For a full list of conditions for which Omega-3 has a benefit, to those where it is proved to have no benefit, we have a ready-made solution from the US National Institutes of Health. (Just click and read on), if you are curious to know more.

3.    Always read the label.  There are only two omega-3 oils that seem to have any potential medical benefit; eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).  Nobody seems to know which is better than the other or what the optimal ratio is.  To do much good to your heart, the research shows you need something like 2g of EPA/DHA daily, note that 2g = 2000 mg. 

Now go look on the label of those expensive fish oil tablets you have in the bathroom cabinet.  For a start you can forget about Omega-6 oil, your diet already has way too much and also ALA, you do not need any more of that either.  It also looks like any Omega-9 is not going to do much either, your body can make that itself. Omega-3 and Omega-6 oils are considered “essential” fatty acids, since your body cannot make them, and it does need them.  Western diets have far too much Omega-6 and too little Omega-3. It seems that the ration is often 10:1, when it should be much closer to 1:1.  Processed junk food is full of omega-6.

 

 

one capsule contains  180 mg of EPA /DHA ( no data given is it mainly EPA or DHA)

one capsule contains 192 mg of EPA / DHA (24g EPA and 168g DHA)

 

Eye q liquid.  5ml contains 244mg of EPA / DHA (186g EPA and 58g DHA)

• Entire 200ml bottle has 9.8g EPA/DHA.
• 500g of farmed atlantic salmon contains 10.7g EPA/DHA

 

If you do want to give EPA/DHA to your child why not give them fish to eat?  It may be true that tuna and swordfish have high levels of mercury, this is because they are large fish.  Large fish eat small fish and then accumulate mercury.  Large sea fish tend to be very expensive and beyond your budget anyway.  There are smaller cheaper fish that are full of EPA/DHA.  The U.S. Department of Health and Human Services (go on, click it) produces a great list of hoe much EPA/DHA is in 80+ types of fish.  Note that tinned tuna has almost no EPA/DHA because it is cooked before it is canned.

 

• A cheap fish like farmed trout has 1.15g EPA/DHA per 100g
•  Herring has even more oil; it has 2g EPA/DHA per 100g

•  Farmed salmon has 1.2g EPA/DHA per 100g

•  Don’t forget sardines, anchovies, mackerel, whitebait etc.

 

Depending on where on the planet you live, the price of both supplements and fish varies greatly; but by my calculations it is much cheaper to eat the fish.  Fortunately for me, Monty just loves to eat all kinds of fish, not just fish fingers.

 

Conclusion

 

There is currently no proven scientific case to give expensive omega 3 supplements as a treatment in autism.  It would be pretty straightforward to conduct such research; the fact that it has not been done, must tell you something.
 

There is a single interesting study that has not been replicated.  Even that study used dosage  levels of EPA/DHA that are 6 times higher than the supplement makers are recommending.  So a EUR 20 bottle of Eye Q would last you just 6 days.

 

There is plenty of evidence that fish is good for you and your son.  So just eat fish, and plenty of it. Maybe it will help with his autism, maybe not; it is certainly much healthier than red meat, processed meat and even his favourite chicken nuggets.

 

 

 

 

Rats in the Basement - lab update #1

This may be only the 4^th post on this blog, but in the background research is actually quite far advanced.  A few hundred learned papers on, have there been any further epiphanies?

Well at the risk of sounding smug, I have to say yes, or least maybe.

 

When I started out in late January 2013, I knew that rats in the basement was not going to be an option; either my elder son would use them for target practice, or my wife would object.

My original plan was to rely on my powers of observation to guide my research and just draw on the pool of existing scientific research as needed to develop a plausible hypothesis, that could then be tested and quite likely rejected.  This is more like primary research, the fun type. I used to do a lot of this.  Primary research is used extensively in the business world and sometimes verges on espionage.

In primary research I now have two projects:

 

·         TRH and more specifically TRH analogs.  This looks very promising, but gets pretty complicated and there will be lots of citations.

·         Hypokalemic Sensory Overstimulation.  This may prove to be just a curiosity.

Secondary research is what most people do.  It is all about reading other people’s research and then either dutifully regurgitating it, or putting a new spin on it and taking it forward.  I used to this a lot and it can also be fun.  The interesting thing I learned is that two different people, or “expert” teams, could look at the same data and come to diametrically opposing conclusions.  This has great relevance to Applied Neurological Analysis, which as from post #1 is now officially known as ANA.
 

Researching TRH took me into the depths of research concerning a wide range of psychiatric disorders, addictions, epilepsy and even HIV-AIDS.  It also led me to read some much lighter weight studies that actually did have the word autism in them.  Then one evening, on Google Scholar, I was jumping between Hyperbaric treatment for autism and vitamin B12 injections and had about 20 windows open on my laptop.

 

Just as lithium-ion batteries can overheat and start smoking on Boeing 787s, it is also possible with your laptop.  Not wanting my research to be grounded, I picked up the pace.

 

I was reading a paper that was in effect junking the use of Methylcobolamin (Methyl-B12) injections in autism.  Then I saw that it mentioned a subgroup for which it appeared the therapy had indeed produced a measurable  positive effect.  The author hypothesized that in these children the B12 was somehow raising the level of Glutathione (GSH). A-Ha and what exactly is that?  All will be revealed in a later post.

 
This led to 2 developments:-
 

·         Open up an investigation into GSH

·         Note that sub-groups can exist in autism and so there just may be more to a “failed” clinical trial than meets the eye.

 
Having allowed the laptop to cool down, I did a trawl through the research on Omega 3 fish oil.  I am not a follower of Complementary and Alternative Medicine (CAM), but it turns out that its followers are big buyers of fish oil.

I used to take omega 3 capsules because I read they are good for your heart.  A friend recently asked us to pick up some special ones in London that are supposed to make your kid get higher marks at school.  It turns out that even my Mum used to be given cod liver oil and malt during World War 2.  I would have written “during the war”, but in many parts of the world, where you read this blog, it then raises the question “which one?”.

Having learned from my friend Colin, that you can actually be allergic to specific kinds of fish, I had discovered a few months back that I too have intolerance to farmed salmon and trout.  When I looked into what they feed the fish, I soon came to believe that this was a plausible cause of my symptoms.  So this means no more salmon and much less “natural” omega 3.  It turns out that some people are even allergic to the fish oil supplements as well, but thankfully not me.

I concluded that I have a ready use for a large batch of unwanted, long expiry dated fish oil, should I need one.  So I decided to add an Omega 3 to my secondary research and potentially add it to the primary research pile.  I do admit to starting with a sceptical bias.

As you can see, often you need both primary and secondary research for the same job, but for the moment at least, there are no rats in the basement.

 

 

P.S.

If a further dose of humour is required at this time of day, ponder the reaction of the Japanese airline executive from ANA (All Nipon Airways) who is googling to see how much PR he is getting due the Lithim-Ion batteries in his parked fleet of Boeing 787 Dreamliners. Colin will be famous in Japan, as he deserves to be, and the sales of fish oil will rise.