Tuesday, 25 June 2013

Too Much Protein..Really? (Part 1)

It is often reported (and with very good reason!) that everything should be taken in moderation. This is nowhere more true than with factors that affect your precious self! So, needless to say that media reports suggest an effect a deleterious effect of overconsumption of the overtly masculinised, required macro-nutrient, protein.

You’ve probably heard that too much protein is not good. Reported by media outlets and your mother or father (I know mine do!) too much protein puts stress upon your renal system and causes bone calcium excretion. This isn’t just a housewives tale however, but has credence in that this evidence was drawn from good quality published articles.

BUT ladies and gentleman, it is my feeling that this knowledge requires an update and until that time no conclusion can be made as to protein and its negative effects upon the renal system and bone calcium health.
So let’s break down my reasoning by looking at the studies cited as the evidence for not consuming more protein than the RDA..


Protein and Renal Disease


This is a classic case of media outlets causing a hubbub while taking information out of context. The main point of debate is that an excess intake of protein above the RDA causes chronic renal disease through increased glomerular pressure and hyperfiltration. The data for this is sound enough, with the frontier study that caused the media excitement being that of Barry M, et al, 1982.

This article is methodologically well put together and is deserved of its title as a frontier study (that which leads the way, as being the first study, for further research in its field). However, picking it apart (unfortunately it’s behind a paywall: http://1.usa.gov/1aLkB0j) I came to realise the incorrectness of its use as a study to back up protein moderation in a healthy individual.

  1. The majority of the evidence used is cited from animal models.
  2. Another group of evidence collection is that of patients with co-existing renal disease.
  3. No healthy individuals are used as an evidence model.


Therefore, I conclude that this study is not suitable to be used in order to draw association between increased protein intake and renal disease onset.


Don’t want to take my word for it?


Why would you? But there are published article’s out there without the media spotlight upon them that back up what I’m saying:

Martin W, et al (2005): Concluded that –

Although excessive protein intake remains a health concern in individuals with pre-existing renal disease, the literature lacks significant research demonstrating a link between protein intake and the initiation or progression of renal disease in healthy individuals.”

Further, Martin went on to say –

there is not sufficient proof to warrant public health directives aimed at restricting dietary protein intake in healthy adults for the purpose of preserving renal function.

Knight E, et al (2003) designed a prospective cohort study (which is a study using a group of individuals and following them from the outset to the end of the study, measuring predetermined outcomes overtime. These usually include both a control and treatment group). It was concluded that high protein intake was not associated with renal function decline in women with normally (healthy) operating kidneys.

Blum M, et al (1989), in a study using both vegetarians (a group which is demonstrated to have lower protein intake) and non-vegetarians, both displayed similar deterioration in renal health with age. It concluded no difference in age, sex, weight and kidney function between groups.



Kidney health and the bodybuilder's diet?


You may be reading this and wondering whether any studies have been conducted regarding us (a very broadly termed "us"). Us athletes and our high protein diets to aid weight loss, or high protein diets and resistance training or endurance. 

Well, to the best of my knowledge, no credible studies have focused in on these topics. However, what can be taken away from this to begin with is that at the current time, no authority should be warranted towards decreasing protein intake in order to maintain renal function.

In my opinion, it would appear that protein intake over the RDA, even so far as 1.4-2g/kg (a range commonly stated as that required for exercising individuals) of bodyweight show no risk factors for decreased kidney function, in healthy, exercising individuals. It should still be prudent to mention that those individuals with mild renal insufficiency should monitor their intakes more closely, as evidence shows that protein intake may be closely related to the progression of renal disease.





Well, that went on for a bit longer than I thought it might today! I’ll be bringing you part 2 as soon as I can, debunking protein intake linked to decrease bone health. In the meantime, if you have any thoughts or could highlight any studies relevant to increased protein intake (over 100g per day) regarding kidney health, I’d more than appreciate taking a read!

Friday, 21 June 2013

HMB - The Conclusion

So here’s a recent article I dug up while reading through the most recently published papers from the JISSN (for those of you not “in the loop”, that stands for the Journal of International Sports Science Nutrition), ‘International Society of Sports Nutrition Position Stand: beta-hydroxy-beta-methylbutyrate (HMB)’. Let’s see what you think to what they have to say.


What is HMB?


So, if you may not know, HMB (I’m not going to lengthen this word any more than necessary!) is a metabolite of leucine (one of those golden boy amino acids). Its most praised effect is its ability to exert an antiproteolytic effect, therefore to halt the break-down of muscle protein.
                This was first shown all the way back in 1996 when this exact antiproteolytic effect was demonstrated in resistance exercise training. Along with this it is also reported to increase lean muscle and strength gains. This first paper advocating its potential as a supplement for resistance exercise used a strong methodology, using varying doses of 0, 1.5g and 3g, and 69 subjects.


Sceptical Science leads to firm conclusions!

A “scientifically significant” stamp of approval is not placed upon something from one study alone it should be realised. In science, a sceptical eye should ALWAYS be used. There’s no time one shouldn’t be careful. 

However, we like to think that the journalists and publishers have done their research too so we don’t have to! Nevertheless, aside from looking through the methodology yourself and checking the strength of their conclusion, another way is by repeats. Repeatable studies showing similar results (which can be quantitatively shown through meta-anaylsis) can lift us past the huge haze that surrounds supplements and their usefulness!

So this is basically what the JISSN have done. They’ve brought together a number of studies and qualitatively (this means without using statistical analysis – which doesn’t necessarily take away any credence) concluded that HMB:

  1. Speeds recovery from high intensity exercise. 
  2. Dose should be 1-2 grams, 30-60 minutes prior to exercise and 60-120 minutes prior to exercise, dependent on the type of HMB (HMB-FA and HMB-Ca respectively).
  3. It may require a “build-up” in the system for the effects to become noticeable. JISSN suggest a dosage of 3 grams for two weeks prior to a resistance workout (You should notice recovery increased efficiency after two weeks of taking then basically).
  4. It may also prevent loss of lean body mass when dieting (catabolic situations).
  5. It may also be of benefit to the elderly, due to its antiproteolytic nature.


I thought I’d get the conclusion out the way first – not very proper I know! Anyway, what I’d like to mention for a paragraph, or two, are the differently bound forms of HMB, Ca and FA.


HMB-Ca and HMB-FA:

HMB-Ca is the only form you’ll find in the supplement market to date. It is HMB in its calcium salt form and found as a powder (often placed within gelatine tablets). The other form, HMB-FA stands for “free acid” and is used in research in gel form, containing a buffer to raise its pH to 4.5 before ingestion.
                Due to HMB-Ca being the only commercially available form on the supplement market only small amounts of research have been specifically done using the free acid form. However, of the research conducted, the results are surprising:

  1. FA doubled peak plasma levels of HMB in one quarter of the time of that of Ca (30 minutes in comparison to 120 minutes).
  2. Concentrations over 180 minutes was 91-97% greater in FA than Ca.
  3. Half-life 3 hours compared to 2 and a half hours (FA and Ca respectively).
  4. The most significant finding was that after analysis of plasma clearance (indicating levels of tissue uptake and utilisation) it was found that it was 25% greater with HMB-FA consumption.



This does lead to an intriguing question – when will the “new formula” HMB, that supplement companies are sure to brand this as, come out?
                In that we may soon see a new gel form of HMB..  and if we do, you now know exactly what the gel form is!





Want to take a look at the article yourself? -  http://www.jissn.com/content/10/1/6#B7

Tuesday, 29 May 2012

Medium Chain Triacylglycerides (MCTs) - The Under the Radar Fat with Above Bar Health Benefits!

As promised, it's time for some MCT (medium chain triacyldlyceride) talk!

I was talking to a friend the other day who works in the animal nutrition industry. Specifically, he and his team are tasked with coming up with agricultural improvements in efficiency, in particular increased feed efficiency of livestock (ie feed used more as fuel rather than stored as fat - therefore increasing the proportion of lean (muscle) mass).
          If you don't already know, agriculture is the industry to get into at the moment. It's not at all farmers and tractors, speaking with an accent and digging up vegetables. The truth is, the study of Agriculture includes research and development into a number of significantly important processes which will be required in order to maintain our constantly growing world population, taking into account the limits imposed by natural and man-imposed areas for food/livestock growth and production.

Agricultural Science includes research and development in:


  • Production techniques (irrigation, nitrogen soil input)
  • Improving agricultural productivity; quantity and quality (drought-resistant crops and animals, new pesticides, yield-sensing technologies, crop growth models, cell culture techniques)
  • Transformation of primary products into end-consumer products (production, preservation, and packaging)
  • Prevention and correction of adverse weather, environmental and man-made antagonists to farming and production.
In Conlusion, Agriculture is at the forefront of future development and production efficiency. Without efficiency we will not be able to support our exponential World population growth (which is estimated to reach 9 billion of 2050 - currently ~7 billion).

So, how does this ramble relate to MCT's? Well..one method my friend mentioned in terms of improving food efficiency, thereby increasing lean proportion of overall body weight.

I realised then that my knowledge of fats did not stretch as far as I would have liked! So, obviously I researched as much as I could in a frenzied fashion (after my exam of course!!) and managed to delve into a topic which does not receive nearly enough mainstream media (or even cooking channel!) attention, in my opinion.

In general, you are taught that the longer a chained fatty acid is, the healthier it is for you. The longer chained fatty acids 18+ all include double bonds, therefore making them either mono- or unsaturated fatty acids. This distinction leads led to the concept that doubly bonded fatty acids are healthier for you than saturated fatty acids. Generally, this is the case.

HOWEVER..

This is not always the case, and there are exceptions. Most notably you may have heard of 'trans' fats in the news and their prevalence in cardiovascular disease and general heart health dis-effects. Well, a trans fat is only a trans fat if it has a single double bond in the trans position on the chain (remember, the trans simply tells us the conformational state of the fatty acids double bond in relation to the hydrogen atoms surrounding it).
          As you may realise then, a trans fatty acid is actually a trans mono-unsaturated fatty acid. An example would be Vaccenic Acid (C18:1), the prevalent trans fatty acid found in dairy produce fat and human milk.

So there are exceptions in terms of fatty acid's being healthier in the doubly bonded state, and, as you can guess, there are exceptions in the non-doubly bonded state. Most prevalent of which are the class known as the MCTs (medium chain triacylglycerides).

Medium Chain Triacylglycerides:


To be considered 'medium' the fatty acid must consist between 6 and 12 fatty acids. The most prevalent are:
  • Caproic acid (C6 = 6 carbons) - found in goat's milk
  • Caprylic acid (C8) - coconut oil, goat's milk, palm kernel oil.
  • Capric acid (C10) - coconut oil, goat's milk, palm kernel oil.
  • Lauric acid (C12) - high concentrations in coconut oil, palm kernel oil, human and goat's milk.
Alright, now that we have the sources and 4 prime MCT's labelled and out the way, let us get into the nitty gritty of how they are unique.


MCTs in Energy & Exercise:


The first real quality of MCTs is their lower calorie content than their longer chain sisters. They carry 8.3 calories per gram in comparison to LCTs 9.4 calories per gram.

But this is just the kicker. More importantly, the reduced chain length means there is a much more rapid metabolism of the nutrient as a fuel. The end result of this means that the calories within MCTs are much more readily and efficiently converted to fuel instead of storage as excess adipose (fat) tissue.
          This efficiency is thought to be due to MCTs being able to directly cross the mitochondrial membrane, and not requiring a mediator to aid membrane passage, as LCTs do (shown as the Hepatocyte -> LCFA pathway in the diagram).
          The result is an excess accumulation of acetyl-CoA. This acetyl-CoA is then fed into multiple metabolic pathways in order to synthesise the production of ATP. The excess is fed into the production of ketone bodies (generally only produced in low carbohydrate diets in order to maintain normal brain glucose levels, as free fatty acids cannot cross the blood-brain-barrier - therefore, conversion to ketones is required).

Since the 1980's, separation of MCTs from food sources has been common practice, causing MCTs to be a common food supplement, specifically to those interested in enhancing energy levels and endurance within high-intensity exercise.

In animal studies it has been shown countless times how MCT supplementation increases physical endurance. Fushiki et al, 1995, carried out one of these research projects. The design parameters were based around a swimming endurance capacity test in mice. Those mice supplemented on MCTs were found to out-perform the non-supplemented mice. It was noticed that muscles of supplemented mice contained higher levels of key metabolic intermediates within the Kreb's cycle (primary energy production mechanism). 

MCTs in Weight Control:


In terms of controlling weight MCTs have a 3 pronged approach:
  • Lower calorie content than other fats
  • Minimally stored as fat
  • Enchanced metabolism due to thermogenic properties associated with them (therefore = more calories burnt!)
Another benefit is that they cause the accumulation of excess Acetyl-CoA, which in turn leads to production of Ketone Bodies. Now in general, Ketone bodies are associated with extended periods (generally 3 days plus) of low carbohydrates (<50g per day). However, as seen, ketone production begins pretty much instantaneously in MCT intake. Therefore, it gives credence to the idea that results may be seen more rapidly in those carrying out 'keto' diets and also more easily adhere to the diet.

Studies on both animal and human studies have shown conclusive results and both concur with each other.

Human:
(Scalfi et al, 1991) Researchers fed six lean and six obese young males meals containing either long-chain triglycerides (LCTs) or MCTs plus LCTs. In both the lean and obese individuals, post-meal thermogenesis (fat burning) was enhanced after consuming meals containing MCTs.

A number of studies support the benefits of using MCTs in weight loss programs to boost energy levels and increase fatty acid metabolism to aid in reducing fat deposits.
           In one study (Hainer et al, 1994), when researchers in Czechoslovakia treated 60 obese patients with MCT oil they concluded that MCTs offered a number of benefits, stating, 
“Administration of… medium-chain fatty acids can…improve the long-term success of diet therapy of obese patients.” 

 MCTs in Appetite Control:


An obvious benefit to any person trying to restrict dietary calories!
         In one 14-day study, six healthy male volunteers were allowed unlimited access to one of three diets: a low MCT diet, a medium MCT diet, and a high MCT diet. Caloric consumption was significantly lower on the high MCT diet. The researchers noted that substituting MCTs for other fats in a high-fat diet,
“can limit the excess energy intakes and weight gain produced by high-fat, energy-dense diets.” 





MCTs have also been implicated in a preventative measure against atherosclerosis. They are noted for having anti-coagulation properties as well as lowering cholesterol levels in rats (Stewart et al, 1978). Further, they are reported in having anti-oxidant properties and also hypo-(low) glycemic effects (lowered blood glucose) effects, making them a useful supplementation for diabetics or those at risk of metabolic syndrome.

This gave credence to the possibility that a diet higher in MCTs increases the life-span of animal models.

A further testimonial to MCTs benefit in heart health is from Sri Lanka. Census reports, from 1978, detailing deaths per million from ishaemic heart disease (the gradual occlusion of arteries, leading to myocardial infarction) were 1 (per 1 million). Comparing this to most other countries, their values varied between 38.4 and 187.7.
           What is the significant dietary fat in Sri Lanka? That's right..Coconut Oil!

To Conclude..


It's great! An under-used, under-talked about fatty acid that really should be given some prominence in the media to raise awareness of the benefits.
          There are a couple of points of gentle warning if you consider supplementing with the MCT oil:

  • Beginning use can cause nausea and gastric discomfort, however, this soon passes and can be easily overcome by starting with extremely small doses (1/4 teaspoon several times a day!), and then gradually increasing dosage as tolerancy increases.
  • It can be used as a salad dressing and cooking oil, BUT be wary as MCT should not be heated to beyond 150 degrees Celsius. This will oxidise it and break it down, therefore affecting taste.

Apart from that! 

  • Increased endurance
  • Rapid absorption rate
  • Thermogenic effect
  • Quick conversion into energy
  • Used post-workout! Huh? A fat after workout? Yes, that's right! It rebuilds muscle and prevents protein degradation.
So, what's stopping you? Well..for myself, I would go out and get some. Indeed I had the intention, but after seeing the price of coconut oil at my local supermarket..maybe when I have a proper job!!



References:

Fushiki T, Matsumoto K, Inoue K, Kawada T, Sugimoto E. Swimming endurance capacity of mice is increased by chronic consumption of medium-chain triglycerides. J Nutr 1995 Mar;125(3):531-9. 


Hainer V, Kunesova M, Stich V, Zak A, Parizkova J. The role of oils containing triacylglycerols and medium-chain fatty acids in the dietary treatment of obesity. The effect on resting energy expenditure and serum lipids. Cas Lek Cesk 1994 Jun 13;133(12):373-5.

Scalfi L, Coltorti A, Contaldo F. Postprandial thermogenesis in lean and obese subjects after meals supplemented with medium-chain and long-chain triglycerides. Am J Clin Nutr 1991 May;53(5):1130-3.

Stewart, J.W., Wiggers, K.D., Jacobsen, N.L., Berger, P.J. Effect of various triglycerides on blood and tissue cholesterol of calves, J Nutr, 1978, 108: 561-566.

It's official, I'm almost back for good!

1 One week and a half..that's all that is left until my last exam is over. But, that's a week and a half in which I can take it a little easier, as it is also my LAST exam.

So, that means, more content, starting right now. I'll be getting onto writing an interesting proposition I read a week or so back about the introduction of greater levels of MCTs into your diet.

An MCT, or medium chain triglyceride, is an atomically smaller form of the normal TAG (triacylglycerol) in the diet, which is LCT (long chain triacylglyceride).

They have proposed life longevity benefits as well as their lower calorie content per g than their long chain sister. Other benefits include:

  • Lack of storage in fat cells
  • More rapid induction of satiety
  • More rapid metabolisation to be used as as energy source
  • Multiple other health benefiting implications 
  • Reduced symptoms of metabolic syndrome seen in obese patients after supplementation for 8 weeks.
So, all this to come! I'll be starting it immediately, so hopefully it'll be up in around 2 hours!

-Tom

Tuesday, 22 May 2012

Arachidonic Acid and the Prostanoids: Our Protection from Within (Part 1)

Another, hopefully informative post here!

In my opinion, nutrition comes hand-in-hand with a good understanding of basic physiology. Physiology itself covers all aspects of the human body, how organs work together, how you move, how you respond to stimuli, perception and just general how the body works. 

SO, I'm going to be covering another aspect of physiology in this post, or more accurately, endocrinology. 

This post will be covering: PROSTAGLANDINS.
(If you can remember back to the  fatty acid - background post, prostaglandins are synthesised from essential fatty acids! )

The post will be split into two, the first page will include: 

Structure and Biosynthesis
           -arachidonic acid cascade
           -cyclooxygenases (COX)
                 -COX inhibitors (non-steroidal antiinflammatory drugs)
Prostanoid receptors
• Prostaglandins and physiological systems

           -Stomach
           -Kidney
           -Cardiovascular
           -Brain
           -Uterus

Prostaglandins are synthesised from phospholipid precursors (arachidonic acid is liberated from phospholipids by enzyme phospholipase A2 (PLA2)) and are implicated in the control of many physiological processes. They are a family of 20 carbon molecules, with four double bonds, derived from arachidonic acid (AA). Also synthesised from arachidonic acid are thromboxanes. 

Prostanoids = prostaglandins and thromboxanes.

Another Eicosanoid,  (lipid mediators synthesised from a 20 carbon essential fatty acid; arachidonic acid) as well as prostaglandins and thromboxanes, are leukotrienes.

Leukotrienes are involved in the immune system, in particular in asthma and allergic diseases. Incidentally, lipoxygenase inhibitors are used to treat asthma.

Source of Prostanoids
The Arachidonic Acid Cascade

The diagram to the right shows the conversion of arachidonic acid to eventual prostaglandins (PG) and thromboxanes (TXA). The COX enzymes occur as either constitutive (always present) (COX-1) or inducible (COX-2)

AA --> PGG2--> PGH2 --> synthase or isomerase enzymes --> PG / TXA

As a side note, aspirin is a non-selective inhibitor of the COX-1 and COX-2 enzyme. Therefore inhibiting synthesis of prostanoids. It is therefore used as a treatment for chronic joint diseases, anti-inflammatory properties, analgesic and antipyretic properties. However, it has been implicated with side effects:
  • Gastrointestinal ulceration and bleeding
  • Renal damage
  • Platelet dysfunction
Inhibition of COX-1 has undesirable side effects (as stated above!). Therefore, effort has been put into finding compounds that will selectively inhibit COX-2 enzymes only. Several of these have in fact been synthesised (Coxibs). At the same time, there has been an increased risk of cardiovascular disease associated with coxibs.

These selective inhibitors of COX-2 enzymes are referred to as non-steroidal anti-inflammatory drugs (NSAIDs). They give symptomatic relief in the treatment of osteoarthritis, rheumatoid arthritis and short-term treatment of post-operative pain.

The prostanoids a tissue produces depends upon the synthases it expresses (examples will be covered later!)


Catabolism of Prostanoids (breakdown):

Most Prostaglandins are rapidly inactivated by PG specific enzymes within organs. Inactive products are further degraded by general fatty-acid oxidising enzymes.

These PG specific enzymes are most highly present in the lung. The half life of most PGs in the circulation is <1minute. 


Prostanoid Receptors:


There are 5 main classes of G-protein coupled prostanoid receptors.  

They activate various intracellular signalling pathways (eg adenylate cyclase and phospholipase C)

The sensitivity to prostanoids is determined by the relative distribution of the 5 classes of receptors present within a tissue.









Prostaglandins and Physiological Systems:


The Stomach:

PGs have motility, secretory and protective effects on the gastrointestinal tract. They act on the smooth muscle of the gut from the oesophagus to the colon.
  • PGE2 and PGI2 are synthesised in the gastric mucosa (COX-1)
    - they act to increase mucus and bicarbonate secretion
    - also act to decrease acid secretion
    - finally they also cause vasodilation (an increase in blood flow)
  • They protect the stomach against damage
  • Therefore, inhibiting this COX-1 enzyme takes away the protection the stomach previously had, making gastrointestinal excessive bleeding a risk. COX-2 inhibitors cause less damage to the stomach than the non-selective COX enzyme inhibitors (for example, aspirin).
The Kidney:

PGs in the kidney act to modulate the haemodynamic and excretory function.
  • PGE2 is found in the medulla of the kidney
  • PGI2 in the glomeruli.
Synthesis is stimulated by ischaemia (lack of oxygen), angiotensin II and antidiuretic hormone.

Under normal, basal, conditions synthesis is low, however when vasoconstrictors are released (eg angiotenin II) PGE2 and PGI2 cause a compensatory vasodilation.





The Platelets:

Platelet aggregation (build up) is caused through the production of TXA2 (Thromboxane) through the COX-1 enzyme. Its biosynthesis is increased in syndromes of platelet activation (unstable angina, myocardial infarction (heart attack), stroke).

The opposite of platelet aggregation, platelet blocking, occurs through the production of prostacyclin (PGI2) from the endothelial cells.

Hence, prophylactic treatment for thromboembolic diseases (those causing platelet aggregation, therefore formation of multiple thrombi) is half an aspirin a day (blocks COX-1, therefore no platelet aggregation as normal).

The Cardiovascular System:

PGs control the contraction of the underlying smooth muscle, influence platelet formation/non-formation and cell function. 
  • PGI2 relaxes smooth muscle and inhibits platelet aggregation by activating adenylate cyclase (through G protein coupled receptors, therefore upregulating cAMP levels = nuclear response initiated).
  • PGE2 synthesised from microvessel endothelial cells. It acts as a direct vasodilator and inhibits noradrenaline release from sympathetic nerve terminals.
  • The net effect = DECREASE total peripheral resistance and blood pressure and INCREASE perfusion (delivery of blood to capillary bed).
The Brain:

COX-1 and 2 present in various brain centers. PGE2 and PGD2 are both produced in the brain and the spinal cord.
  • PGE2 stimulates the thermoregulatory center in the pre-optic area, leading to fever (PGE2 release stimulated by pyrogens. Aspirin decreases these systems of fever.
  • It is involved in synaptic signalling, neuronal firing, neurotransmitter release, nociception (pain response) and appetite.
  • Altered brain arachidonic acid production has been implicated in neurological, neurodegenerative and psychiatric disorders.
The Uterus:

Endometrium and Myometrium both synthesis PGs. 
  • PGF2alpha is generated in large amounts
  • PGE2 and PGI2 are generated by the uterus and act as vasodilators.
  • E and F PGs contract non-pregnant as well as the pregant uterus. The sensitivity to PGs INCREASES during gestation.
  • NSAIDs can delay labour
PGs play a role in dysmenorrhoea (painful menstruation). This increases the production of both PGE2 and PGF2alpha.

PGs also play a role in menorrhagia (excessive blood loss)
  • Increase vasodilation and decrease haemostasis
  • They also increase generation of PGI2, which impairs haemostasis and causes vasodilation.