Traitorous Fatty Acids Tuesday, May 3 2016 

or  Is One Lipid Unhealthier Than Another?

Pretty much everyone has heard of omega-3s.  Health geeks will probably be able to go further and name DHA and EPA as omega-3 fatty acids.  It is also well-known that these are poly-unsaturated fatty acids.  But why should these be more special than others?  And are those others therefore bad?  And why are there different ones anyway?

The answer to last of those questions is that fatty acids come from several different sources—plants, fish, mammals, birds—that live in different environments and thus that have different requirements of their fats.  This is reflected in the molecular structure of the fatty acids, and thus which sort they are.

The answer to the second question is that is that no fatty acid is intrinsically bad as such, though if we consume more of them than we use the result is an increase in the volume of fat stores, leading to obesity in the long term.  So, there is a limit to what we need regarding fat.

The answer to the first question is that there are some fatty acids we need for certain things that others cannot really substitute for.  DHA is well-characterised in this regard.  For example, there is evidence that it has a role in human behaviour1, 2.  Adolescent children who are at risk from bipolar disorder have lower levels of DHA and EPA1, as do younger children with ADHD2.

It does not stop with children who are already unwell.  There is mounting evidence that  these poly-unsaturated fatty acids have a role in cognition not only in children3, 4, but also in adults with dementia5.  Evidence drawn from groups of a wider age span suggest that it affects cognition throughout life6.

So, one might conclude that a supplement of DHA and EPA and we can knock ADHD, bipolar disorder, dementia and being a bit crap at spellings tests or the crossword, on the head.  This would be easy to organise; such supplements are amongst the most easily available of any that are commercially available.  Sadly, this is naïve.  However, it is not immediately obvious why this should be.

Evidence has begun to emerge that not all children who have plentiful DHA and EPA in their diets exhibit the same good cognition as others who have the same amount but live elsewhere.  This encouraged investigators to dig deeper.  One factor that has appeared is that people who live in places where a higher fat diet is more common, tend not to exhibit the cognitive benefit of DHA and EPA.  One study in particular was conducted with populations from 28 countries, taking into account other factors such as wealth as well, showed this correlation neatly3.  This work concluded that omega-6 fatty acids in effect drowned out the omega-3s, suggesting that the right ratio of the two would give good results.

But what is the magic ratio?  This has also been researched3, 7, 8.  It seems that humans evolved for a diet of a ratio of about 1:1 of omega-6 to omega-39, though up to about twice as much omega-6 as omega-3 is still regarded as optimum.  This can also be written as a ratio of up to 2:1 linoleic acid to the sum of DHA and EPA.  Some of the western diets investigated showed a ratio of around 50:110 with an average of around 16:19.

This invites a second level of finger wagging from dieting know-it-alls: not only should we eat less fat in order to tackle obesity*, but virtually no omega-6 fatty acids either.  In theory, this should be easy to implement.  Our bodies are able to make saturated fat and can produce unsaturated fats from saturated ones with enzymes called desaturases.  We only really need things like DHA and EPA in our diet because in practice we cannot really make them.

This theory is helpful, but once again the next step is not necessarily intuitive.  Which foods fit into this mould and which do not?  The table below shows data on the fatty acid profile of oils from various foods11-13.

fatty acids in foods

 

I think I will have salmon for lunch.  And hold on the sunflower oil in the mayonnaise.

 

 

References

*Some dieticians, quacks and faddists argue that (bang on about) a low carbohydrate diet is a good way of losing weight.  Lowering carbohydrate intake can reduce the calorific intake.  However, it contains less than half the number of calories per gramme as fat.  So if an individual ingests more calories than they use, lower carbohydrate intake may be a less strong way to reduce overall calorific intake.

1. R. K. McNamara, R. Jandacek, P. Tso, T. J. Blom, J. A. Welge, J. R. Strawn, C. M. Adler, S. M. Strakowski and M. P. DelBello, Early Intervention in Psychiatry, 2016, 10, 203-211.

2. A. Crippa, C. Agostoni, M. Mauri, M. Molteni and M. Nobile, Journal of Attention Disorders, 2016.

3. W. D. Lassek and S. J. C. Gaulin, Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA), 2014, 91, 195-201.

4.K. W. Sheppard and and C. L. Cheatham, The American Journal of Clinical Nutrition, 2013, 98, 659-667.

5. M. Loef and H. Walach, Journal of Nutrition in Gerontology and Geriatrics, 2013, 32, 1-23.

6. M. Weiser, C. Butt and M. Mohajeri, Nutrients, 2016, 8, 99.

7. C. Hoyos, C. Almqvist, F. Garden, W. Xuan, W. H. Oddy, G. B. Marks and K. L. Webb, Asia Pac J Clin Nutr, 2008, 17, 552-557.

8. S. Yehuda and R. L. Carasso, Proceedings of the National Academy of Sciences of the United States of America, 1993, 90, 10345-10349.

9. A. P. Simopoulos, Biomedicine & Pharmacotherapy, 2002, 56, 365-379.

10. M. A. Martin, W. D. Lassek, S. J. C. Gaulin, R. W. Evans, J. G. Woo, S. R. Geraghty, B. S. Davidson, A. L. Morrow, H. S. Kaplan and M. D. Gurven, Maternal & Child Nutrition, 2012, 8, 404-418.

11. C. Blanchet, M. Lucas, P. Julien, R. Morin, S. Gingras and É. Dewailly, Lipids, 40, 529-531.

12. M. Enser, K. G. Hallett, B. Hewett, G. A. J. Fursey, J. D. Wood and G. Harrington, Meat Science, 1998, 49, 329-341.

13. J. Orsavova, L. Misurcova, J. Vavra Ambrozova, R. Vicha and J. Mlcek, International Journal of Molecular Sciences, 2015, 16, 12871-12890.

 

 How Hot is Hot? A Burning Question About a Hot Condiment Thursday, Jan 19 2012 

Plenty of people like a good hot curry. I am not one of them, but I think that most people have met, or know, someone who likes wolfing down the hottest curry in the house as a matter of pride. I do know someone who likes to munch on the same kind of hot curry but exquisitely slowly. Either way, it is safe to assume that pretty much anyone who has had a strong curry, and either enjoyed it or not, will remember the flavour forever.

There has even been a certain amount of study on this topic: some time ago, the compound capsaicin (Figure 1) was identified as the cause of the hotness. Several related compounds have also been identified, some of which are ‘hotter’ than others. This led to the desire to measure the ‘hotness’, resulting in the Scoville Heat Unit, and the Scoville Scale.

There is also the well-known opportunity for a schadenfreude with curry flavours. As it can be a strong flavour, when someone bites on something unexpectedly teeming with chopped jalepeños, the shock on their face is palpable. However, this shock can also be turned on its head with respect to public order. Recent anti-capitalist protests in America have given rise to some disturbing images of people sprayed with a capsaicin formulation (commonly known as pepper spray) either intentionally, or apparently not.

While these are shocking, and the mental and physical distress caused by the use of this ‘riot-control agent’ are readily understood, other factors are also important. The use of pepper spray as a weapon of self-defence, against a rapist or criminally violent attacker for example, seems not unreasonable. However, the link between pepper spray and deaths in people exposed to it who also have compromised respiratory function, increases the interest in managing the use of pepper spray, both politically and scientifically.

Figure 1. The structure of capsaicin, showing a more polar section (left) and a more lipophilic one (right), giving rise to a comparison with lipid structures.

One way of taking things further is to understand the science behind what is happening when pepper spray is used. A judgement can then be made about safety and appropriate conditions for use. The structure of capsaicin (Figure 1) suggests that it has a lot in common with what we know about lipid structure – a relatively polar (hydrophilic) section as one end, and a lipophilic hydrocarbon chain as the other. However, it is not just the lipid-like properties of capsaicin and its related compounds that give rise to the effect we remember so readily – after all, we eat lipids of one sort or another in almost every mouthful and most do not have the same effect as a vindaloo on our taste buds. This hot sensation is due to an effect of the capsaicin on nerves that feel heat (thermoception) and pain (nociception).  Recent work has suggested that there is a direct impact on the activity of calcium channels in nerves and earlier work has found that such exposure was responsible for permanent damage to the cells involved.This is quite sobering when looked at from a riot-control angle. If a chemical is able to cause innervation, as measured by pain, it is arguable that it is a drug. If it is a drug, strict licensing laws would apply. This also influences the dose(s) that can be used legally. Perhaps we need to reflect on the use of pepper spray of indiscriminate dose, as a crowd control agent?