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Newsletter April 2014 – A question of Fats

 Ok – this is a summary of some recent research and ideas around fat intake. Make a nice cup of tea, grab some dark chocolate and some coconut oil and enjoy! It’s a lot to read so set aside a little time.

Contents

  • A fat lot of good – Why should we care?
  • Saturated fats – the craziness of correlation
    • Problems with correlational studies
    • Why were saturates shunned?
    • Later PUFA/Med diets – good for overweight
    • Later, better meta-analyses
    • Fat for athletes – fat adaptation
    • Coconut oil, the faster fat
    • Fish oils – a stressor or karmar?

A fat lot of good – Why should we care?

Fat is a loaded word. For years, this energy-dense macronutrient has been blamed for all of the incidences and consequences of our obesity epidemic. In the midst of our obesity-epidemic, we need to do as much as possible to encourage good habits and avoid passing on problems to the next generation; the number of adipocytes can increase in childhood and adolescence, though the amount is usually constant in adults. Adolescents can increase their number of adipocytes (fat cells), thus priming them for a lifetime of hefty consequence, although interestingly, individuals who become obese as adultshave no more adipocytes than they had before. But surely these natural foods cannot be solely to blame for obesity when our body has mechanisms in-built to burn fat and use it to fuel our activity. What’s so “good” about good-fats, and why are the “bad fats” so bad? Are these definitions even useful nowadays? Read on and I’ll help you skim over the evidence…

 

Saturated Fats – The Craziness of Correlation

Chowdury, (2014) Association of Dietary, Circulating, and Supplement Fatty Acids With

Coronary Risk A Systematic Review and Meta-analysis. Ann Intern Med. 2014;160:398-406.

The topic of this month’s newsletter was inspired by the much reported release of a landmark meta-analysis of previous trials regarding fat intake. It was one of the largest and most significant meta-analyses in this area, assessing 32 observational studies on fatty-acids from dietary intake, comprising of 530 525 participants. It also included 17 observational studies (25 721 participants) of fatty acid biomarkers; and 27 randomized, controlled trials (103 052 participants) of fatty acid supplementation.

In observational studies, the relative risks for heart disease when comparing the highest dietary intakes of various fats with the lowest were a measly 2% increase in risk from consuming saturated fats, a 16% increase for trans-fats, and surprisingly, a 1% increase for polyunsaturates. A 1% protective effect for monounsaturated fats was found, along with a 7% effect for long-chain n-3 polyunsaturated fats. When looking at the risks associated with circulating fatty acids (rather than just reported intakes), saturates saw a 6% increase in risk as did mono-unsaturates (such as those from olive oil!), and a 5% increase from trans-fats. Omega 3 decreased risk by 16%, and polyunsaturates by 6%. Basically, the risks from consuming trans fats were negligible, and even the links with circulating levels were pretty low! Not only did this trial prove noteworthy enough to conclude that current advice over fat intake may need to be revised, but this study was done in collaboration with the British Heart Foundation and The Medical Research Council and received funding from conglomerates such as Pfizer and Nestle.   However –this correlational study just re-affirmed one thing to me; that we shouldn’t take too much stock from correlational studies! Why was this trial seemingly in opposition to current health advice? Was anything new “discovered”? Let me explain…

 

This trial was BIG. It looked over many previous results on many people. But most of the studies assessed were correlational –they look for trends in large groups of people. This is always subjects to a common mistake – assuming that one thing has caused the other. If we saw firemen at multiple fires, it would be a bad move to assume that fireman were starting them. Is it that saturated fats cause obesity in themselves, or that previous studies have found that people who eat poorly and cram burgers down their throats (yes – high in saturates… as well as sugars and simple carbohydrates) are fat? A similar issue was encountered in a famous trial linking skimmed milk to cancer. Deeper analysis revealed that the skimmed milk drinkers were wealthier, better educated, and saw their doctors more frequently, meaning they were more likely to try to eat healthily, but also more likely to get diagnosed with disease. This current meta-analysis was better placed than most to spot real trends due to the large numbers involved, but dealing with these numbers also means it’s hard to look at sub-groups and look deeply into the data – there’s just too much of it! For what it’s worth, the authors tried to account for “heterogeneity” (differences in outcomes), by comparing studies with similar demographics/durations etc. There was a large amount of variation in the effect of saturates in different trials, but interestingly, there was only a trend linking even-numbered saturated fatty acids with heart-disease – these are synthesised in the body. There was no link for odd numbered saturates (consumed in full-fat dairy) and disease (Figure 2, below). Being overweight and having high levels of fat in the blood was more indicative than intake…

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figures 1-3 showing associations with intake, circulating fats and supplements highlighted by the Chowdry review (taken from Chowdry, 2014)

This brings us neatly to the next problem encountered with epidemiological studies on fat intake – the stats are only as reliable as the data.  Most of the studies assessed would have assessed dietary intake by means of dietary recall. In these days of rapidly escalating obesity rates and poor eating, using one person’s recollection of their last 24hrs’ food-intake as a genuine estimate of their habits over the last is not a reliable method! Furthermore, even biochemical measures of circulating fatty acids don’t tell us about peoples’ diets with any real certainty. High levels of fats are found in people who are obese – even if they got fat from eating sugar. Likewise, saturated fats will be elevated in the blood of overweight populations from fatty acid synthesis.

To summarise, this trial doesn’t tell us a whole lot more than what we knew already. The very slight trends for cardiac risk from eating saturates are negligible when one considers the unreliable nature of the data collection, but it would be wrong to say that they’re particularly healthy. Dietary intake often links junk-food to poor health (unsurprising!), and overweight people are more likely to have high levels of saturated (synthesised themselves) fats and even monounsaturated fats in their blood.

 

So… in this case, why were saturates ever made out to be the bad-guy?

Drug company conspiracies? National Health Strategies, that are linked to big-agriculture-business, bent on selling us grains? No – only joking. No-one wanted to mislead or misinform… but people pay too much attention to correlational studies (so don’t go out and change your healthy diet just on the basis of this paper, either!).  Some of the misguided dietary guidelines emanated from studies such as the Framingham heart study. The Framingham Study was initiated in 1948 with a cohort of 5209 men and women, 30 to 62 years of age, who were then followed up over the course of their lives. This enabled some well powered, large-scale studies that found correlations between saturated fatty acids and cardiovascular disease. However, as more data became available, the associations become weaker. Posener (1991) looked at two groups of males, aged 45 to 55 years (n = 420)and 56 to 65 years (n = 393) over a 16 year period.  Percentage energy intake from saturated fatty acids had a marginally significant positive association with heart disease, although significant positive associations were also found with total fat intake, and monounsaturated fatty acids in the younger cohort. The associations remained even after adjustment for cardiovascular disease risk factors, including serum cholesterol level, suggesting that their effects are at least partially independent of other established risk factors… or, that the links between dietary reports and circulating fats are also tenuous! None of the dietary lipids were associated with CHD in the older cohort. To shed more light on the problems with dietary reporting, dietary lipids were assessed through “a single 24-hour recall at the initiation of follow-ups” – a single 24-hour recall after 16 years! In this environment of fat-phobia, it is unlikely people will have given 100% accurate descriptions of their yearly food consumption, particularly regarding their fat intake, in a single session with an unknown dietician.

 

Another big problem when assessing not only dietary intake studies, but more controlled trials (say where patients have been provided known foods at a hospital) is individual variation. Different people have very different versions of genes involved in transporting and metabolising fats, but sadly even these associations are currently inadequate for accurately predicting cardiovascular risk. A recent paper on Greek men (Katsiki et al 2014) underlines both the large genetic variation and difficulties faced in making predictions for coronary heart disease. They looked at variation in apolipoprotein (apo) E genes, and other genes encoding fatty acid metabolising proteins, such as I405V (V, I) and Taq1B. Whilst the TaqIB (B1, B2) polymorphism affected plasma low-density lipoprotein cholesterol levels in overweight men, and the I405V (V, I) polymorphism affected triglyceride concentrations in normal weight men, no correlation was found between BMI, disease-state and any of the polymorphisms. Very often, genes may predict “risk factors” for disease (high levels of cholesterol, say), but these “risk factors” themselves area again only correlated with a risk of disease and aren’t 100% accurate. Larger reviews of the literature would seem to highlight fairly regular associations, the major one being over the apo-E gene. Compared with individuals with the ε3/ε3 genotype, ε2 carriers have a 20% lower risk of coronary heart disease, whilst there are also approximately linear relationships of apoE genotypes with LDL-cholestreol levels (Bennet, et al., 2007).

The Mediterranean Diet and the Promise of Polyunsaturates

As stated previously, dietary intake studies are very poorly controlled and inaccurate. However, analysis of circulating fatty acids may also be misleading, as there is often uncertainty as to whether these were synthesised in the body, or elevated due to consumption. These findings are even harder to interpret if studies include overweight people, as their fatty acid metabolism is now pathological. For example, Chowdry’s meta-analysis above highlighted a protective association from monounsaturates on cardio risk, but strangely found that blood levels of oleic acid (found in olive oil) were a risk-factor for disease. This is in conflict with one of the largest most recent multicentre trials, the PREDIMED trial.

Lasa (2014), Comparative effect of two Mediterranean diets versus a low-fat

diet on glycaemic control in individuals with type 2 diabetes; European Journal of Clinical Nutrition 1–6

Lasa looked at the effect of dietary counselling towards achieving a “Mediterranean diet” on 191 overweight, diabetic participants at risk of CHD (77 men and 114 women, aged 60–80).  These overweight participants (BMI=30) were randomised into two Mediterranean diets supplemented with virgin olive oil or nuts, or into a standard “low fat” dietary group, based on current health advice. Although overweight, participants were free of cardiovascular disease; but showed type 2 diabetes and had poor levels of circulating cholesterol. They were followed up after 1 year, and in both Mediterranean diet groups, but not in the low-fat diet group, there was a significant reduction in body weight. However, the flaws of dietary reporting are again highlighted, as further analysis suggests that the Mediterranean dieters actually ate significantly more and lost weight, compared to the weight-stable “low fat diet” who consumed a greater calorie-intake. An earlier study on these participants revealed that those on Mediterranean diets not only lost weight, but were less likely to re-gain after 3 years.  Although there was no significant difference in weight-regain between groups, average regain tended to be lower in the Mediterranean diet-groups. Higher antioxidant capacities in the blood were also significantly associated with a reduction in body weight after 3 years among subjects allocated to the virgin olive oil group. Again, though, the PREDIMED studies arerely on reported food intake. Dietary regimes were meant to be followed after an education session, and although the Spanish males studied were probably not unfamiliar with the Mediterranean diet, their high BMIs suggest a previous lack of dietary restraint and dietary control!

To look further into studies on Mediterranean diets, Mente (2009) conducted a meta-analysis on randomised trials and saw protective associations of this type of diet on cardiovascular disease. He used the Bradford Hill criteria (1998) (strength, consistency, temporality, and coherence) to attempt to analyse the likelihood that a Meditteranean diet  was at all responsible (although, as we’ve said this will never be a particularly valid method when looking at correlations!). However, there were no relationships with specific fatty acids, just the dietary intervention that included “high intakes of vegetables and nuts with cheese, milk and lean meats”.

 

To investigate the biological effects of different fats in a bit more depth, I started with a recent, very informative review by Krishnan and Cooper (2013) whish directed towards some good science.

 

Sridevi Krishnan · Jamie A. Cooper (2013); Effect of dietary fatty acid composition on substrate utilization and body weight maintenance in humans; Eur J Nutr DOI 10.1007/s00394-013-0638-z

In a meta-analysis comprising trials on obese and healthy subjects, they analysed studies that compared monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), and saturated fatty acids (SFA), measuring the biological impact alongside the longer term health effects. Firstly, they studies diet-induced thermogenesis, or the fat vurning effects of foods. Many of the analysed trials involved feeding a high fat diet for several days, then looking at the effect of specific fatty acids in stimulating fat-oxidation after a meal.  While single-meal studies show that saturates jave less of a fat-burning effect compared to unsaturated fats, noth MUFA and PUFA seem to be more effective at stimulating energy expenditure, according to  studies using labelled fatty acids assess exogenous  fat oxidation (Jones et al), as well as those measuring breath gases (clandinin et al). Thier review of long-term dietary interventions also support the notion that unsaturated fats induce greater energy expenditure, and are effective in aiding weight-loss when used to replace saturates in the overweight.

More conclusive results could be gained from looking at more controlled trials where food is actually provided to the participants. These are expensive and less frequently carried out, but where this is the case, a higher intake of olive oil and monounsaturates seems to be associated with improving cardiovascular health.

One such trial looked at replacing saturates with monounsaturates, with diet being completely controlled by the lab over 7 week study (berglund, 2007):

Berglund (2007) Comparison of monounsaturated fat with carbohydrates as a replacement for saturated fat in subjects with a high metabolic risk profile: studies in the fasting and postprandial states. Am J Clin Nutr 2007;86:1611–20.

Berglund studied slightly overweight participants at risk from adverse effects of low fat diets (fifty-two men and 33 women; high insulin, low HDL, High LDL/TG etc etc), and put them on differing weright-maintenance-diets. The “average American diet” was used as a control versus a “MUFA diet” (where 7% of energy from saturated fatty acids was replaced with monounsaturated fatty acids); and a a higher carb diet (7% of energy from saturates was replaced with carbohydrates). Replacing saturated with monounsaturated fats or carbohydrate reduced LDL cholesterol, whereas circulating fats tended to be lower with the MUFA diet, but were actually significantly higher with the higher carb diet. More and more it seems that replacing saturated fats in the overweight with a high polyunsaturated diet improves cardiovasvular health.

 

But it this due to the effects of a single group of fatty acids? Unlikely. As I said before, we should be looking at improving dietary patterns, and the Mediterranean diet focuses on “high intakes of vegetables and nuts with cheese, milk and lean meats”. Hardly revolutionary!

 

Although the effects of monounsaturates from dietary intake and circulating levels seems to be uncertain, all controlled trials where healthy Mediterranean diets have been provided, consisting of higher intakes of olive oil and a healthy, vegetable-based , have shown a positive impact.

 

To conclude, we should be advocating:

  • A high intake of vegetables
  • A high intake of nuts
  • Protein recommendations advocating:
    • cheese
    • milk and
    • lean meats
    • Higher intakes of olive oil and monounsaturates may be particularly beneficial for combating obesity in the overweight
    • The one plausible “bad guy” may be the trans-fat, consistently associated with p[oor health with no positive findings associated with its consumption (see figure 1-3)

 

 

 

 

 

 

 

 

 

 

 

 

Fat and athletes – Fat adaptation

So fats are neither good nor bad, but useful in a certain context. This is certainly the case in sport, where fat offers a great deal of energy for athletes, although is less effective at powering explosive, anaerobic exercise. As with all things fatty, this is an area of much controversy. I’ll start with the good news…

 

Sawyer, J. C., R. J. Wood, et al. (2013). “Effects of a short-term carbohydrate-restricted diet on strength and power performance.” J Strength Cond Res 27(8): 2255-2262.

Just before Christmas, Sawyer (2013) studied the effects of carbohydrate depletion on power athletes reducing their body weight. Although these athletes train at high, carbohydrate-dependant intensities, often their short sharp sessions are not threatened by glycogen depletion.  31 strength-trained individuals (16 men and 15 women, averaging 24 years old) took part in a cross-over trial of weight-reduction whilst being tested for performance (hand dynamometry, countermovement vertical jump, 1RM bench press and back squat, maximum-repetition bench press, and 30-secondWingate anaerobic bicycle test). Body composition was measured with the unreliable bioelectrical impedance method.  Athletes were subject to baseline testing, then again after 7 days on either habitual diet (40.7% carbohydrate, 22.2% protein, and 34.4% fat), then finally after 7d  carbohydrate-restriction (5.4% carbohydrate, 35.1% protein, and 53.6% fat). Performance was maintained, with a trend to improvement after carbohydrate=depletion (grips strength, jump height and squat strength).  Wingate performance also improved insignificantly. However, there was no randomisation in the order of the diets, (carb restriction always followed the habitual diet) meaning learning and training effects cannot be discounted. Also, the diets were not energy matched (2,157 vs 2,537Kcal per day), further clouding conclusions.

There was no significant difference in fat-free or fat-mass after carbohydrate restriction compared with a habitual diet considering all of the athletes. It does seem however, that strength and power gains are supported by protein over and above carbohydrate, and particularly in athletes undergoing weight-loss, providing protein throughout carb depletion can preserve performance.

 

The aim in sports nutrition for years has been to fuel athletes more efficiently with fat to allow the preservation of the muscles’ high-intensity glycogen reserves; the more fat you can burn, the more carbohydrate you can save for a sprint finish. However, the trade off seems to be a compromise with intense performance Up-regulating the body’s fat-oxidsing enzymes often comes at the expense of those responsible for anaerobic, high-intensity, carbohydrate-metabolising adaptations.

 

Older studies (Helge, 1996) show fat-adaptation to have a negative impact on performance after 7 weeks training, obstructing adaptation in previously untrained athletes… Even after 1 week’s carb-loading fat adaptation compromised performance by impairing carbohydrate utilisation:

 

Helge, J. W. (2002). “Long-term fat diet adaptation effects on performance, training capacity, and fat utilization.” Med Sci Sports Exerc 34(9): 1499-1504.

After 7 weeks of training, HR and noradrenaline were significantly higher during exercise after the fat-rich diet. This increased activity in the sympathetic nervous system was maintained after switching from the fat rich diet to the carbohydrate rich diet for 7 days, even after muscle glycogen concentrations were restored. Similarly to studies on “depleted state training” aerobic biochemical adaptations (shown by Vo2max values) increased similarly in both groups – fat adaptation being just as beneficial for aerobic adaptation. After 7 weeks of fat-adapted training, glycogen as measured with biopsy decreased, and bmarkers of fat fuelling increased.   However… after the week of carbohydrate loading, a lot of the benefits of fat adaptation seemed to be lost or outweighed by shortfalls in glycolysis. Although carbohydrate oxidation was lower compared to fat in the fat-adapted group at 7 weeks, this was restored after the week of carbohydrate feeding. Muscle glycogen break-down during exercise was equal in both fat and carbohydrate trained participants after 7 and 8 weeks, driven by intensity, rather than by training-nutrition. Performance (time to exhaustion at 85%), went from 35, to 104min with carbohydrate supported training. In fat training, it went from 35min to 65min after the depleted state training, then increased to only 78min after the carb-loading week. Clearance of lactate and blood-sugar were impaired, whilst insulin was markedly higher at 8 weeks (a marker of insulin resistance!).  So, in untrained participants it seems foolish to neglect carbs when we want to get fitter.

 

However; trained athletes are essentially fat-burning machines. Perhaps fat adaptation would be more productive in endurance-athletes? Increased rates of fat oxidation without having to focus on enhancing aerobic/ mitochondrial capacity may be better suited to such athletes.This idea was explored by some of the pioneering work by scientists such as Louise Burke, (2000) which essentially showed that 4-7 days of “fat adapting” enhances an endurance athletes already well developed capacity to utilise this fuel.  

Burke, L. M., D. J. Angus, et al. (2000). “Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling.” J Appl.Physiol 89(6): 2413-2421.

Burke studied eight well-trained male national or international level cyclists and triathletes (age 29.3 yr; weight 74.4 kg; V˙ O2 max 64.4 6 1.8 mlzkg21min);  In two trials in a randomized, crossover design with a 2-wk washout period separating each trial. For 5 days they consumed either a high-carbohydrate diet (9.6 g/kg/day CHO, 0.7g/kg/dy fat) or an isoenergetic high-fat diet (2.4 g/kg/dy CHO, 4g/kg/dy fat)  with 1.7g/kg protein while undertaking supervised training, standardised for their aerobic capacity. On day 6, subjects ingested high carb and rested before performance testing on day 7 [2 h cycling at 70%, then a fixed-load time trial (about 30min).

Gas analysis showed carbohydrate oxidation was reduced after fat adaptation. Biopsies confirmed muscle glycogen was spared.  Although time trial performance was lower for fat adapted athletes (34 vs 30min) this trend failed to reach significance. For some athletes, performance was markedly lower, but others were less affected – endurance trained athletes didn’t improve, but weren’t badly affectd by fat-adaptation.

A similar finding was uncovered by Stepto et al., 2002. Seven well-trained competitive male cyclists or triathletes (age 24 yr, mass 75.3kg, V˙ O2peak = 5.0  L/min (66ml/min/kg) were trained to deplete muscle glycogen, completing a 20-min warm-up at 65% of V˙ O2peak, immediately followed by 8 x 5 min work bouts at 86% ofV˙ O2peak with 60-s recovery. These athletes were then split into high fat and high carb groups in the same way as Burke’s study, meaning only the carb-fed athletes could replete glycogen levels.

Fat adaptation diets were effective as shown by gas analysis and post exercise lactate levels only declined in the fat-adapted athletes, showing a decline in glycolysis at a given intensity. Interestingly, although perceived exertion was higher, work volume was unimpaired by fat adaptation vs carbohydrate-feeding. In trained athletes, fat adapting hurts, but they could perform just as as well, even at high intensity…

 

So – to conclude:

  • In well trained athletes, higher fat diets may help throughout weight reduction and will likely improve their ability to burn fat for fuel.
  • Although there are no clear performance benefits, fat-adaptation is unlikely to impair training-adaptation for either endurance or strength/power.
  • Caution should be exercised with regulating training volume to prevent illness and injury, as glycogen depletion may be associated with adverse immune outcomes.
  • Untrained individuals should not be advised to attempt fat adaptation strategies as the risks for injury and negative training-experiences are not even justified with any positive outcomes.

 

 

 

 

 

 

“What about MCTs?” I hear you cry…

If fat oxidation is impractically slow for performance benefits, then what about ingesting a fast burning fat? As early as 1951 it was recognized that MCTs are converted transported directly in the blood, as opposed to being transported as larger “chylomicron” particles. MCTs also diffuse into the mitochondria, stimulating fat oxidation (rather than having to be actively… and slowly transported), and also bypass adipose tissue, which makes them less susceptible to deposition into fat-stores (Bach and Babayan 1982). Seaton (1986) also demonstrated that sedentary participants fed with two different iscaloric meals would oxidise more fat and burn more calories of the fats in the meal were replaced with coconut oil.

 

These health benefits also translate into performance…

Van Zyl, C. G., E. V. Lambert, et al. (1996). “Effects of medium-chain triglyceride ingestion on fuel metabolism and cycling performance.” J Appl Physiol (1985) 80(6): 2217-2225.

Van Zyl, et al. (1996), on three occasions separated by 10 days, arranged for six endurance-trained cyclists to ride for 2 h at 60% of peak O2 uptake before a 40-km time trial. During the rides, the subjects ingested a total of 2 liters of a glucose-labeled beverage containing a random order of either 10% glucose, 4.3% medium-chain triglycerides (MCTs); or 10% glucose + 4.3% MCTs (carb+MCT). Although replacing carb with MCTs slowed the time-trials by about 9%, adding MCTs to CHO improved the time-trials from by an average of 1 minute. Faster time-trials in the carb+MCT trial than in the CHO trial were associated with increased final circulating concentrations of free fatty acids and decreased final circulating concentrations of glucose and lactate.

This trial showed that adding MCTs to ingested CHO reduced carb oxidation and increased reliance on fat; even in the high-intensity Time-trial. Labelled glucose oxidation was the same, these data suggesting that MCT oxidation decreased the oxidation of muscle glycogen. In these endurance trained athletes (already displaying a certain amount of fat-adaptation), then MCTs + carb added an extra, utilisable source of energy. However, these benefits were only obtained by adding the mcts in addition to carbohydrate – this represented an extra 800 calories. The trials were not energy matched, so it could be argued that adding an extra 800kcal of carbohydrate would have also improved performance compared to the control group.

 

This idea was tested by Jeukendrup (1996) who tested two different interventions with the same calorie content, against another intervention with only a marginal calorie increase.

 

Jeukendrup, A. E., Saris, W. H. M., Van Diesen, R. I. C. H. A. R. D., Brouns, F. R. E. D., & Wagenmakers, A. J. (1996). Effect of endogenous carbohydrate availability on oral medium-chain triglyceride oxidation during prolonged exercise. Journal of Applied physiology, 80(3), 949-954.

He trained gave subjects either a 600Kcal of sports drink, a 600Kcal split of 70% carbs and 30% MCTS, or the initial 600Kcal of sports drink with an additional 20g MCTs (an extra 180Kcal) in a crossover trial.  This was drunk throughout a low intensity (50%) 3hr cycle, which should have been ideal for fat metabolism. However, no significant differences were detected in glycogen breakdown among the trials, or mean exogenous or endogenous carbohydrate and fat oxidation. In these trained endurance athletes, providing carbohydrate throughout a prolonged ride undid any potential benefits of the MCTs. Using the same 600Kcal nutritional interventions above (carb, or 70% carb/30% MCTs), and cycling at 50% for 90 minutes, Jeukendrup showed that even prior glycogen depletion didn’t make MCTs more effective at inducing fat-oxidation. There are many rate limiting steps that affect fat oxidation, such include the rate of lipolysis to mobilize fatty acids in adipose tissue, concentration of albumin, use of carrier proteins for uptake, efficiency of lipoprotein lipase and endrenergic receptors, carnitine, as well as carbon and saturation for beta oxidation (Jeukendrup et al 1998). As a result of these rate limiting steps, no glycogen sparing is observed, even when using the “fast burning” MCTs for fuel.

 

What would be an interesting next step is to combine the effects of fat-adaptation with MCT supplementation. It could be that this could create a perfect storm for fat-fuelling performance…

And so finally we come to fish-oils. A favourite of mine for health and athletic advantage, where does the evidence really lie?

 

The proposed mechanism for fish oils revolves around hormones and inflammation. Omega 3 fatty acids provide the precursors for less inflammatory hormones than their omega-6 counterparts, and an increased intake of omega-3 has been shown to shift the inflammatory towards a less inflammatory state. Also, lipids comprise 50-60% of the brain’s dry weight, 35% of which are long-chain polyunsaturates – mostly a fat called DHA. Therefore a combination of improved. However, these poor little fish again suffer from falling victim to correlational analyses, as many of the most useful indications for supplementation don’t come from good quality trials. Researchers such as Cmdr Hibbeln and Prof Simopoulos have correlated fish intake to societies with lower instances of violent crime, depression and suicide – however, when trying to pinpoint the differences in a society’s psyche, there are many other cultural, historical and geographical influences besides their intake of oily fish! Simopoulos has claimed that pre-existing societies consumed omega-3 and omega-6 in a ratio of about 1:1, falling far short of today’s 1:10 ratio with a western diet. Where he managed to find an ancient Babylonian to study, analyse his red-blood-cell fatty acids, and ask him to write his food diary, I don’t know. Perhaps in the same town that those Paleolithic leviathans have detailed their dietary secrets! What I’m alluding to is that food diaries are unreliable, and estimated ones are just fanciful. Correlational studies are speculative – what we need is science.

 

Fish oils and inflammation in athletes

What is fairly well proven is that consuming high intakes of long chain omega 3 (that from fish, not flax-seeds and vegetarian sources) can influence inflammation and oxidative stress. What is less certain is the impact on performance. No trials have yet shown a performance impact from supplementation, although rehabilitation and various health markers may be improved.

It would seem that in trained athletes training sufficiently intensely to illicit a notable inflammatory response, high doses of fish oils(EPA and DHA of approximately 1–2 g/d, at a ratio of EPA to DHA of 2:1), may be beneficial in counteracting exercise-induced inflammation as shown by decreased levels of CRP and cytokines such as TNFa. However, there are inconsistencies between trials and no performance benefit have yet to be shown, although athletes suffering from inflammatory conditions such as exercise-induced asthma have been seen to benefit from less symptomatic training (Mickleborough, 2003).

 

Lembke, P., J. Capodice, et al. (2014). “Influence of omega-3 (n3) index on performance and wellbeing in young adults after heavy eccentric exercise.” J Sports Sci Med 13(1): 151-156.

Recently, sixty-three healthy male and female college students (mean age 18.8 years) were randomised in a 2:1 ratio to receive fish oil supplementation (n=42) or placebo (n=22). Receiving High DHA fish oils or placebo (2.7g total DHA+EPA; 300mg EPA, 2400mg DHA) participants then were analysed  for their “omega index”, a measure of red-blood-cell omega-3 content.  After 30 days supplementation without training, the authors assessed the impact of a single session of eccentric forearm extensions (two sets x 30 reps). Measurements over 4 days revealed a reduction in pain at both 72 and 96 hours in subjects with a higher omega-3 Index.

There was also a significant lowering of post-exercise blood-lactate levels and improved emotional POMS scores (emotional stability), as well as a statistically significant reduction in CRP levels in subjects with a higher N3 Index after 24 hours. Subjects with a higher Omega-3 index also reported less pain related to DOMS at 72 and 96 hours post-exercise (but no functional differences in torque/strength). This paper pretty much sums up the current state of affairs over fish oils – well being and inflammation seem to improve, but nor real performance benefits have been recorded.These findings are similar to those found by Bakhtyar et al (2011) in 45 untrained male participants after 2 months of supplementation and a single exercise session.

The experimental group showed less elevation in TNF-α and PGE2 immediately, 24, and 48 hours after exercise, when compared with the other groups, whilst significantly less elevation was shown in the concentration of IL-6, CK, and Mb for the experimental group at 24 and 48 hours after exercise. Inflammation was successfully regulated, and lactate metabolism also controlled for 48 hours after exercise. But no performance benefits… Inflammation is a useful biological response and instils training adaptations. It may be that the benefits in a clinical setting are not the same for athletes who either depend on such high levels of inflammation, or at the very least are accustomed to them throughout their day to day training.

 

Cognitive function in athletes

Fish is brain food, right? There have been many studies in those with poor diets, developmental disorders and criminal tendencies that correcting fatty acid imbalances with fish oils can help brain functions. However… what about in normal people? And what about in athletes? It seems from recent studies that fish oil supplements can help athletes’ cognitive abilities in a useful way for sport. One of the best controlled, valid trials on athletes was that of Guzman et al (2011), who assessed the impact of 24 3.5g/day DHA-rich fish oil on 24 female soccer players from two Spanish Super League teams.

Guzmán (2011) Journal of Sports Science and Medicine DHA- rich fish oil improves complex reaction time in female elite soccer players, 10, 301-305

Participants were tested using a validated test of reaction time (in fact a driving simulator used by the Danish government to re-qualify banned drivers!) after 4 weeks of supplementation throughout their normal football training. Fish oil supplemented players showed a significant improvement in the neuromotor function and complex reaction time.

 

So, fish oils may regulate inflammation and support brain functions. But what’s even more contentious is the effect of fish oil supplementation on oxidative stress. It may be assumed by some that as fish oils are anti-inflammatory and attenuate damage from training, they would by extension show antioxidant activity.  However, as these fatty acids are unsaturated, they are essentially more fragile and prone to attack. As they work by incorporating themselves into our cells (where they can influence the production of inflammatory hormones), then there remains the possibility they make our cells finely tuned, but fragile structures, prone to oxidative degeneration. A recently published trial aimed to quash these worries, but was not without it’s own methodological flaws…

 

Capo (2014) Diet supplementation with DHA-enriched food in football players during training season enhances the mitochondrial antioxidant capabilities in blood mononuclear cells Eur J Nutr DOI 10.1007/s00394-014-0683-2

The authors in this study conducted an 8 wk randomized double-blind trial on the effect of fish oil supplementation on oxidative stress. 15 male football players consumed 1g DHA per day, along with other fatty acids and vitamin E in an almond-milk drink.  Throughout pre-season football training (a high eccentric component, but varied and uncontrolled in intensity), 2 groups of n=6 and n=9 were evaluated for levels of oxidative enzymes and damage.  DHA increased superoxide dismutase protein levels after acute exercise, and reduced the production of ROS (ROS production by stimulated blood-cells) after acute exercise. The training season significantly reduced the catalase activity in the placebo group, whereas activity was maintained in DHA group. However, the enzyme glutathione peroxidise (GPx) significantly increased in activity both in placebo and in experimental groups. The authors concluded that there may have been an antioxidant effect of fish oils, and that previous studies that suggest a pro-oxidant effect of fish oils may have been affected by the lack of protective vitamin E as included in their trial. However, the lack of a standardised, highly damaging training protocol limits these conclusions. Oxidation wasn’t directly induced from exercise, instead being induced in a test-tube assay, and the impact of fish oil supplementation may have been exaggerated here as there was no real dietary control, but a roughly Mediterranean diet with high MUFA intake and a low intake of n3 PUFA before intervention.

Antioxidant effects of fish oils have also been found in endurance athletes after a standardised test at 60% maximal-intensity (Poprzecki, 2009), and in resting levels of oxidation in recreational Karate-fighters (Farzanegi, 2012). However, the issue with oxidation would seem to become a problem at higher intensities. One trial to find a negative impact on inflammation was one on elite judoists (Fillaire, 2010).

 

Filaire et al (2010), Effect of 6 Weeks of n-3 Fatty-Acid Supplementation on Oxidative Stress in Judo Athletes. Journal of Physical Activity and Health, 2010

20 male national-level judo competitors were randomly assigned to receive a placebo or

Omega-3 (600 mg EPA and 400 mg DHA) over a  6 wk training block. Training 9 hr/week, including full-combat, this was a real test of inflammation. In addition, they were tested with a standardised judo training session of 2 hr duration that consisted of judo-specific drills and fighting practice with exercise intensity kept between 85–90% VO2max. A significant reduction vs placebo was noted in circulating triglycerides for the omega-3 group after supplementation, an indication of healthy fat metabolism. However, elevated levels of oxidised lipids were found in the omega-3 group after supplementation with no change in the placebo group as well as a significantly greater NO and oxidative-stress increase with exercise.

 

To summarise:

  • Fish oils have yet to enhance any type of performance, although have acutely improved rehabilitation and cognitive function in athletes
  • Fish oil supplementation may help athletes with chronic inflammatory disorders (such as exercise asthma or over-reaching)
  • In lower intensity training protocols or at rest, fish oil supplementation may help support healthy antioxidant processes
  • In better trained athletes, fish oil supplementation may even increase levels of oxidative stress.
    • However, this may not be a negative occurrence
    • Trained athletes exhibit higher levels of oxidative stress throughout training and may need these to adapt

 

 

 

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Categories : Fat Loss
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I met a taxi driver last week and I normally like to hear their stories. This fella had lost 3 stone recently after having being diagnosed with type II diabetes.
It is often during random moments like these when you are engaging with people that different insights crop up and sometimes I can find ways to help people.
Here’s how our conversation went.

taxi_1360265b

‘Great work fella, I muttered, how did you do that?’

‘Ate more chicken, thank god for chicken’, he replied.
‘More veg too. Stopped drinking pints in the week’.

Do you still drink now?

‘Yes, half a dozen on Sundays usually.
I don’t’ want to stop it’s my social time.’

‘Probably good idea to carry on mate, what else did you do?’

‘Stopped snacking between meals, just 3 square meals each day.’

Cool, what you eating for breakfast?

‘Porridge, banana’

(What it is about porridge for breakfast I do not know but so far I’ve not met anyone who hasn’t
gotten leaner when they switch to proper porridge in the morning, I tend to avoid porridge
for clients who are looking to lose weight quickly)

‘I eat fish a couple of times a week also’

‘Fish is good for diabetes’ I tell him.
‘The metformin helps too’

‘Yes I think it does mate, it’s hear it’s quite safe too.
Did the Dr. put you on B12?’

B12, what’s that?

It’s a b-vitamin, metformin stops you absorbing it.

‘Ok, I wonder why the Dr didn’t tell me’

‘Probably didn’t know, anyway mate, pick some up this afternoon it’ll probably save your life ’

What’s it do then?

‘Central nervous system, blood and brain health, reaction time, that kind of thing’

‘Ok I will do, thank you’

‘No problem’

‘Taxi drivers don’t get alzheimers you know?’
‘No mate, I hadn’t heard that.’

‘Yes it’s true – on account of using the brain a lot.’

Ok (I’ll google that one later).

POST TAXI RIDE RESEARCH

Found a couple of nice little articles;
I couldn’t find an article that proved that Taxi Drivers don’t get Alzheimers.

However following the theme of using your brain and cognitive decline … It does like you can teach an old dog new tricks, and the hippocampus can grow with new intensive learning. However this appear to only apply to black cab drivers who have to follow ‘the knowledge’ a 3-4 year study period learning all the roads in London apparently equivalent to a degree  in terms of difficultly.

It wouldn’t, unfortunately apply to my cab driver who was using a Sat Nav. Another reason to stay good at map reading.

As we  age it also becomes important for well being to continue to learn new stuff, it’s sad when you see older people spending their time glued to the TV.

More on the cognitive decline tip, it really does look like a healthy heart makes a healthy mind. More reason to clean up your act in mid-life and start drinking a little more coffee (maybe).

As with all illnesses prevention is better than cure, we don’t yet know all the reasons why there are growing numbers of degenerative type diseases and Alzheimers is a big one. I’m pretty certain that nutrition has a big part to play that’s a reason why I tend to eat well and use supplements in order to try and future proof myself from these potential problems.

 

 

 

http://www.wholehealthinsider.com/newsletter/new-predictors-cognitive-decline/?utm_source=WHI&utm_medium=house_email&utm_term=all&utm_content=news&utm_campaign=WHI_20140327

 

 

 

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