Transfats the Last Bastion of the "Bad Fats"!? Two New Studies Shed Some Light onto Their Impact on Your Health.

Image 1: The Meet the Fats campaign is part of the stultification... ah I mean educational program of the American Heart Association

Meanwhile, even mainstream dietitians are beginning to understand that fats, which have been a, if not THE staple energy source in human history are not the bad boys the anti-fat hysteria of the 1980s would make us believe. Even the American Heart Association begins to advocate the use of "healthy fats" as part of a "heart healthy diet" - unfortunately, the AHA guys still lump Sat (that is the obese guy in the left) Trans (that is the sleazy guy in green) together, although the evidence against poor Sat (who obviously represents all saturated fats) is less conclusive than that against Poly, his money-grubbing sister who would do everything for her sponsors from the corn-industry... well, be that as it may, today's charge is against Trans who is accused of arson, or whole body inflammation, to be precise ;-)

New evidence against Trans is provided by two teams of experts, one from Europe (Bendson. 2011) and the Middle East (Dhibi. 2011). In what I personally would consider battery, Nathalie T. Bendson and her colleagues from Denmark and France assigned 52 (formerly ;-) healthy women randomly to receive
either 15.7g partially hydrogenated soybean oil or control oil without any industrially produced  trans fatty acids (IP-TFA) on a daily basis. The results were not life-threatening, but certainly not desirable:

After 16 weeks, IP-TFA intake increased baseline-adjusted serum tumor necrosis factor (TNF) by 12% more in the IP-TFA group compared with controls. Plasma soluble TNF receptors 1 and 2 were also increased by IP-TFA.

With TNF-alpha's role in the modulation of endothelial and vascular smooth muscle cell function as well as endothelial cell-blood cell interaction and "the importance of such alterations for vascular dysfunction, the initiation and progression of atherosclerosis" (Kleinbongard. 2010), Bendson et al.'s asssumption that

the IP-TFA-associated increase in cardiovascular risk beyond the adverse effect explained by changes in blood lipids may be partly due to induction of systemic low-grade inflammation

is possibly correct. Nevertheless, the jury is still out on how bad TNF-alpha actually is, as its role in cardiovascular disease is actually quite ambiguous with the aforementioned low-grade inflammation on the one hand and its ability to protect your heart by ischemic conditioning on the other hand.

Figure 1: Trans fat content of fresh soy oil, oxidized soy oi and margarine (data based on Dhibi. 2011).

More comprehensive evidence comes from a rodent study by Dhibi et al. who fed 48 male Wistar rats one out of four experimental diets which were either high in fat and included 20% fresh soybean oil diet (FSO), 20% oxidized soybean oil diet (OSO) and 20% margarine (MG) or based on the standard chow (control) with a protein/carbohydrate/fat ratio of 17/62/4 for 4 weeks (Dhibi. 2011). The liver function of the rats, as evidenced by the elevated transaminase levels (ALT, AST) and the increases in alkaline phosphatase (ALP) and lactate dehydrogensase (LDH) in figure 2, took a major beating.

Figure 2: Relative changes in transaminases (ALT, AST), alkaline phosphatase (ALP) and lactate dehydrogensase (LDH) in rats after 4 weeks on diets containing 20% fresh soybean oil, oxidized soybean oil or margarine (data calculated based on Dhibi. 2011)

I suppose the sponsors of the American Heart Association won't like this observation, but it is as plain as the nose in your face that even the "transfat free, heart-healthy polyunsaturated soybean oil" led to statistically significant increases in alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) levels... what, ah... of course that is because the diet was high in fat - how could I forget that 20% fat is still way too much and humans, just like rats should eat a 62% carb 4% fat diet ... I guess that was enough sarcasm for one blogpost, so let's back to the facts, now.

Figure 3: Correlation  between  fatty  acid  isomers  in  the  diet  and  oxidative  stress
  parameters in rat’s liver and plasma hepato-specific enzymes (data based on Dhibi. 2011).

The changes in liver function were accompanied by profound reduction in antioxidant enzyme activity (SOD: superoxide dismutase; GPx: glutathione peroxidase; CAT: catalase) and increased accumulation of conjugated dienes (CD) and malondialdehyde (MDA), the respective correlations of which with the fatty acids isomers (trans fats from mono-unsaturated and poly-unsaturated fatty acids, as well as total transfat content) are plotted in figure 3.

Image 2: Rat liver histology.

Due to its scale (only two different transfat profiles, i.e. oxidized soybean oil and margarine) the study's statistical power is yet so small that we can only make a definite case against the total transfat content for decreases in catalase activity and oxidized polyunsaturated fatty acids for the accumulation of conjugated dienes. With correlations in the the >0.5 and <-0.5 range for many other suspects and crimes, I will yet leave it up to you, the jury, to decide, which members of the transfat family (I suppose the American Heart Associations Trans character must have a whole bunch of children, then - just like in every honorable mafia family ;-) are to be held responsible for which of these crimes against health, the ultimate result of which you see in the histological changes in the livers of the rats fed with oxidized soy oil (OS) and margarine (MG)... So, members of the Jury, on the Case of Trans Fatty Acid (and his mafia clan) vs. the Suppversity, what you say?

Three Reasons Why Your Doctor May Falsely Believe Your Kidney, Liver or Heart Were Damaged If You Get Blood Work Done Without Adequate Rest After Intense Workouts

Sometimes lab values are deceiving - specifically if allegedly pathological elevations of kidney, liver and (heart) muscle enzmes are a perfectly physiological reaction to exercise. 

You already know reason #1. The heavily increased creatine kinase (CK) levels I've discussed in a previous article at length may look exactly as if you were about to have a kidney failure.

In fact, the CK-levels can be elevated more than 100-fold after an intense workout (Pettersson. 2008). Accordingly, Mougios, et al. (2007) attempted to develop revised reference values for athletes in their 2007 study. The scientists' test revealed that CK levels of >1000 IU/L in male and 513 IU/L in female athletes would be better cut off levels for athletes who are still training than the regular upper limit of <208 IU/L.

If you want to avoid muscle damage, you may try BFR and hypoxia training.

BFR, Cortisol & GH Responses

BFR - Where are we now?

Hypoxia + HIIT = Win?

BFR for Injured Athletes

Strength ⇧ | Size ⇩ w/ BFR

Training & Living in Hypoxia

Closely related to the CK-levels, which are unquestionably the #1 reason your doctor may want to call an ambulance, despite the fact that all you're suffering from is heavy deep onset muscle soreness, are elevated transaminase levels (see time course of elevation in the Petterson study).

Figure 1: Changes in serum enzyme levels after exercise in trained and untrained subjects in response to 15 minutes treadmill running and an 8k run (Fowler. 1962).

In medicine, the presence of elevated transaminases, commonly the transaminases alanine transaminase (ALT) and aspartate transaminase (AST), are considered to be an indicator of liver damage. In athletes, however, elevated levels of both of these enzymes are - just like elevated creatine kinase levels - a mere sign of exercise induced muscle damage.

As the data from a 1962 study by Fowler, et al. indicates, even 15 minutes on a treadmill can lead to significantly elevated ALT (back in the day the enzyme was still called "GPT") and AST ("GOT") levels. An 8k run can increase ALT and AST by more than 150% (see Figure 1). In that the extent of ALT & AST elevations probably depends on the individuals' susceptibility to exercise induced protein breakdown, which is the actual reason the enzymes which breakdown the protein debris in the liver are elevated.

As it is the case with the creatine kinase enyzmes, many primary physicians and scientists are unaware of the connection and the long-lasting elevations of serum transaminases in response to hard workouts.

Figure 2: In trained marines AST (=SGOT), ALT (=SGPT) react significantly less pronounced (Schlang. 1961)

Against that background it's hardly surprising that Pertusi et al. report in a 2007 paper that the exercise-induced elevations of aminotransferases is also the reason that anabolic steroid induced liver damage has overreported. An overreporting of which the scientists say that is has "in turn, biased physicians against considering muscle damage as a possible cause for aminotransferase elevations (Pertusi. 2001).

Chronically elevated liver enzymes should still not be taken lightly. Even if they don't indicate liver damage, they could be a sign of chronic overtraining. After all, Hunter et al. (1971) were able to show that training reduces the initially exuberant increases of the aminotransferases significantly.

Speaking of not taking lightly, one thing you shouldn't take lightly either is your doctor's suspicion that you may have developed a heart disease. 

More specifically, Elliott and La Gerche have recently been reporting that strenuous endurance exercise (SEE) is associated with acute depression of RV systolic function, thus suggesting that exposure to repeated bouts of SEE can have potential long-term consequences. La Gerche and Claessen argued that left atrial pressure is increased during SEE, thereby increasing pulmonary artery pressure. As Fabian Sanchis-Gomar et al. point out in an editorial comment, they thus stated

"that frequent episodes of increased RV work induced by long-term SEE can promote compensatory RV remodeling, increase myocardial damage biomarkers such as troponins and B-type natriuretic peptide, or even accelerate heart failure (HF)" (Sanchis-Gomar. 2015). 

The Spanish researchers do yet highlight that to the best of their knowledge the bulk of the evidence available supports that the above mentioned alterations which include among other the cardiac-specific creatine kinase marker are rather transient, with a dose-effect relationship existing for exercise intensity and duration.

"Physicians and health professionals should be aware that healthy individuals who engage in SEE sport events could exhibit acute, transient cardiological features that are apparently compatible with cardiac diseases, yet these alterations are attributable in most cases to transient physiological responses rather than pathological status"(Sanchis-Gomar. 2015).

Against that background, it may be a good idea to take two weeks off in order to retest, if your doctor says that your biomarkers suggest that you may be suffering from heart disease.

Read the previous article for all the details on CK elevations.

Bottom line: While you should never take the "bad news" your doctor may have for you lightly. It may be wise to evaluate, whether allegedly pathological changes in creatine kinase (CK), transaminases (ALT & AST) and / or strange alterations in troponins and or B-type natriuretic peptide that suggest you may be suffering from kidney, liver or heart damage may simply be the result of a recent workout.

Since CK, ALT and AST can remain elevated for more than a week (see time course of elevation of AST in Petterson's study), it would be best to take two weeks off of strenuous training before you do a re-test which will then - hopefully - confirm that the disconcerting abnormalities were nothing but a result of your last intense workout | Comment on Facebook!

References:

• Elliott, Adrian D., and Andre La Gerche. "The right ventricle following prolonged endurance exercise: are we overlooking the more important side of the heart? A meta-analysis." British journal of sports medicine (2014): bjsports-2014.
• Fowler, William M., et al. "Changes in serum enzyme levels after exercise in trained and untrained subjects." Journal of applied physiology 17.6 (1962): 943-946.
• Hunter, J. BARRY, and JERRY B. Critz. "Effect of training on plasma enzyme levels in man." Journal of applied physiology 31.1 (1971): 20-23.
• Mougios V. Reference intervals for serum creatine kinase in athletes. Br J Sports Med. 2007 Oct;41(10):674-8. Epub 2007 May 25.
• Pertusi, Raymond., R. D. Dickerman, and W. J. McConathy. "Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?." JOURNAL-AMERICAN OSTEOPATHIC ASSOCIATION 101.7 (2001): 391-394.
• Pettersson, Jonas, et al. "Muscular exercise can cause highly pathological liver function tests in healthy men." British journal of clinical pharmacology 65.2 (2008): 253-259.
• Sanchis-Gomar, Fabian, et al. "Long-term strenuous endurance exercise and the right ventricle: Is it a real matter of concern?." Canadian Journal of Cardiology (2015).
• Schlang, Captain HA, and C. A. Kirkpatrick. "The effect of physical exercise on serum transaminase." The American journal of the medical sciences 242.3 (1961): 338-341.