I asked 8 researchers why the science of nutrition is so messy. Here’s what they said. – Vox

You Can’t Trust What You Read About Nutrition | FiveThirtyEight

The emerging picture on n-6 is that adequate intake is somewhere between 0.5% and 1% of calories with toxicity developing somewhere between 3% and 10% of calories depending on the amount of n-3 stored in the tissue. 
The catch is n-3 is even more volatile than n-6, making safe forms of n-3 supplementation hard to find and placing limits on the amount of supplementation which can be safely consumed. 

The 2015 “Scientific” Report of the Dietary Guidelines Advisory Committee recommended Vegetable Oil as the primary fat despite the fact estimated US consumption of n-6 PUFA is at 9% (probably a low estimate) and 10% is the high end for tolerance (and probably a high estimate). 

There are identified mechanisms tying PUFA excess to cardiovascular disease, liver disease and obesity. These are strong ties (it will happen) not loose ties (it may happen). The only question is at what level and predictions for heart disease tie closely with observations. There are well documented increases in all three diseases since vegetable oil consumption increased. 
Bill Lands: 2014 Review of EFA

Historical perspectives on n-3 & n-6 impact to health.

Healthy intake levels of n-3 & n-6

n-6 involvement in the development of cardiovascular disease.

n-6 and overeating in the development of cardiovascular disease.

Issues with dietary recommendations  
Nutritionists View on n-6/n-3

Outstanding information on the hazards of PUFA perioxidation. 

Followed by perplexing recommendations of mitigating the hazards with anti-oxidant supplementation and n-3 (which is even more volatile than n-6) supplementation. 

The Slow Discovery of Essential Fatty Acids

Details on the original meaning of “essential” when it comes to n-3 & n-6 (necessary for growth rate and skin quality in mice) and details on how hard it is to develop a PUFA deficiency (answer: damage the intestines and place on a zero fat intravenous diet).
Out of Balance You Tube Video

Promotional video by a company selling seafood Seafood bias but well produced and some good info. 

Links between PUFA excess and impact to mental health.

Ties in to the report which came out this week on a rise in death rate for middle age white males. 

Impact to mental health back in 1972.

The Issue:
DGAC: Dietary Guidelines Advisory Committee 

PUFA: Polyunsaturated Fatty Acid

SFA: Saturated Fatty Acid

Every five years a Dietary Guidelines Advisory Committee (DGAC) is formed to review US dietary guidelines. The most recent DGAC released it’s 2015 Scientific Report in February.

The 2015 DGAC report recommends Americans use vegetable oil as their primary source of fat. Here’s the wording from the report:

“In practice, non-hydrogenated vegetable oils that are high in unsaturated fats and relatively low in SFA (e.g., soybean, corn, olive, and canola oils) instead of animal fats (e.g., butter, cream, beef tallow, and lard) or tropical oils (e.g., palm, palm kernel, and coconut oils) should be recommended as the primary source of dietary fat.”

The 2015 recommendation is a more extreme continuation of a recommendation developed in the 1970’s to avoid saturated fat. Americans have heeded the recommendation to avoid saturated fat but relied primarily on carbohydrates as a substitute. The 2015 report found that the shift from saturated fat to carbs adversely affects health and therefore recommends emphasizing polyunsaturated fatty acids (PUFAs) as a replacement for saturated fat. The 2015 report acknowledges there are no studies which show a link between saturated fat consumption and cardiovascular disease.

There are three significant concerns with the 2015 DGAC recommendation:

1) The recommendation is based on statistical analysis of imprecise data and predictions based on computer models. The predictions ignore chemistry.

2) The recommendation is based on an assumption that lowering low density lipoprotein levels by increasing PUFA consumption will reduce the risk of cardiovascular disease. It will not reduce the risk. There is strong evidence it will increase the risk of, not only cardiovascular disease, but also obesity and liver disease.
3) The DGAC recommends replacing a chemically stable substance which has been consumed for millions of years (saturated fat from plants and animals) with chemically unstable manufactured substances (soybean, corn, olive, and canola oils).

The debate over fat is not new. 

Gary Taubes and Nina Teicholz have both published well researched accounts of the gaps in the evidence supporting U.S. dietary recommendations on fat. 

Credit Suisse Research Institute also released a report on dietary fat this year. Although the report is not perfect, it provides a good overview of the evidence against consumption of excess PUFA.

The report can be found here: http://bit.ly/1KwjnFD

Discussion of the Credit Suisse report appears to have been limited to nutrition and financial circles. The general public is effectively numb to any new cries of wolf even though this one is legitimate.

The conflicting evidence should at least give the DGAC pause. It has not. 

In a quote listed in a September 2015 British Medical Journal article, Barbara Millen, the DGAC Chairman, was quoted as saying “we thought we nailed it” regarding the recommendation on saturated fat. When Nina Teicholz asked Alice Lichtenstein, the DGAC Vice Chairman, about the evidence related to low density lipoproteins and heart disease, Lichtenstein replied that it was “complicated” and she “didn’t have time to review it.”

From Bill Lands:

Historical perspectives on the impact of n-3 and n-6 on health

A likely candidate for a very early step in atherogenesis is the repeated postprandial reversible loss of endothelial function [55] and [56] which could occasionally convert into a chronic inflammatory locus. Endothelium-dependent dilation is lower with higher postprandial triacylglycerolemia (a marker for high food energy density). An often-neglected postprandial process when excess food energy forms the much-discussed circulating blood biomarker low-density lipoprotein (LDL) is the hydrolytic release of large amounts of non-esterified fatty acid (NEFA) into the plasma [10]. The biological impact of the much-neglected NEFA and its resultant oxidant stress (indicated in Fig. 3B) may be greater than the effect of the co-produced LDL (with its adherent cholesterol). However, daily messages about LDL cholesterol from marketing and research groups greatly exceed information on the simultaneously released NEFA, and they divert attention away from harmful NEFA actions.

8.1 Actions of non-esterified fatty acids (NEFA) amplified by n-6 mediators

Meal-induced vascular dysfunction and oxidative inflammatory conditions (measured by hydrogen peroxide and isoprostane levels) as well as released monocyte chemoattractant protein-1 were less when diets included fish oil n-3 HUFA [57]. Lipemia-induced loss of endothelial function involves impaired nitric oxide actions, and it can be alleviated in part by supplements of arginine [58]. However, arginine did not prevent an accompanying pro-thrombotic expression of P-selectin and vonWillebrand factor on platelets. Impaired endothelial function monitored as flow-mediated dilation after an oral fat challenge was related to the extent of hypertriacylglycerolemia and oxygen-derived free radicals [59]. Postprandial lipemia was accompanied by increased plasma hydroperoxides and a neutrophil chemotactic agent, IL-8 [60].

Importantly, leukocyte chemotaxis and adhesion are much greater when the mediator is n-6 LTB4 rather than n-3 LTB5 [54]. A significant increase in adhesion of monocytes to the endothelial monolayer occurred in the presence 20:4n-6, and it was decreased with 20:5n-3 [61]. Pro-inflammatory mediators (intercellular adhesion molecule 1, vascular cell adhesion molecule 1, E-Selectin, IL-6, and TNFα) were all significantly increased in endothelial cells incubated with 20:4n-6. Thus, the n-3 and n-6 HUFA proportions in tissues shown in Fig. 3A must be considered when interpreting the impact of food energy density upon risk for CVD shown in Fig. 3B.

Important arithmetic in managing food energy is in balancing intake with expenditure during the course of a day. The on-going societal shift toward a sedentary lifestyle puts a premium on awareness of energy intake and expenditure. During 3 h of typical modern lifestyle activities, a 150 lb person may expend approximately: 225 Cal riding in a car; 202 Cal using computer/internet; 216 Cal watching television; 202 Cal reading book/newspaper; 202 Cal sleeping. Physical activity like walking for 1 h may expend about 270 Cal, and one hour of bicycling, about 500 Cal.

In contrast to low energy expenditure, an average restaurant meal may have 1327 Cal [62], which is 1100 in excess of that likely to be burned in the next 3 h. As a result, much remains for the liver to convert to plasma VLDL and begin the transient process of postprandial endothelial dysfunction. An important, simple tactic to distribute food energy intake more evenly is to eat fewer calories per meal and use small snacks to lower the burden of food energy per hour upon the liver.

With three meals per day and 365 days per year, people may have a thousand postprandial situations per year. If only one per hundred (1%) of these transient postprandial insults converted to a chronic inflammatory site, there might be 10 new sites each year leading to 200 sites in 20 year-old individuals, 400 in 40-year olds and 600 in 60-year olds. Such a low frequency for initiation fits the slow age-dependent histological evidence in the PDAY Study (see Fig. 14 in [10]). While food energy can give reversible pathologies, a more serious process may be the n-6 mediated amplification of transient dysfunction into chronic inflammatory plaques.

The propensity for recruiting macrophages that convert a vascular area into a chronic inflammatory site is much greater when the tissue HUFA balance has a high %n-6 in HUFA. In this way, the higher risk of mortality associated with higher levels of the food energy biomarker, cholesterol (Fig. 1), is seen in populations that have a higher HRA value for the %n-6 in HUFA. A high prevalence of CVD for Americans has remained for decades near 40% for 40-year olds, 60% for 60-year olds and 80% for 80-year olds [63] indicating a failure to prevent the continual disease progression that the PDAY Study showed to begin youth.

Fig. 3A shows how n-3 and n-6 mediators act in CVD, and Fig. 3B shows how food energy intake leads to a high body mass index (BMI) or obesity, which is a predictive associated risk factor for CVD. While factors that cause obesity may also cause CVD, a high BMI per se is not a certain cause of vascular damage, CVD or death. A very large expensive effort to lower CVD by lowering BMI with intensive lifestyle intervention of 5145 overweight or obese patients in 16 study centers [64] gave weight loss through decreased caloric intake and increased physical activity. However, the trial was stopped after millions of dollars and 9.6 years of follow-up showed no lowering of observed risk of cardiovascular morbidity or mortality compared with controls. While many people believe that obesity (high BMI) causes death, the fatal mechanisms and mediators will need to be better identified and prevented if we are to design cost-effective interventions that prevent harm from food energy.

The 2015 Scientific Report from the Dietary Guidelines Advisory Committee (DGAC) was released in February. The DGAC convenes every five years to review U.S. dietary guidelines. The committee submits a list of recommendations to the Secretary of the Department of Agriculture and the Secretary of the Department of Health and Human Services. 

The 2015 report has a significant finding on fat consumption listed in the Executive Summary:

“The DGAC also found that two nutrients—sodium and saturated fat—are overconsumed by the U.S.population relative to the Tolerable Upper Intake Level set by the IOM or other maximal standard and that the overconsumption poses health risks.”

To understand the impact of the DGAC finding, it’s helpful to first get an update on cholesterol.

Much of the confusion about fat, cholesterol and cardiovascular disease comes from lumping two different substances, cholesterol and lipoproteins, under the one term ‘cholesterol’.

Cholesterol is an essential building block for a wide range of substances in the body, from cell walls to Vitamin D. 
Lipoproteins are transport vehicles for carrying triglycerides and cholesterol and can be further divided into High Density Lipoprotein (HDL) and Low Density Lipoprotein (LDL).  LDL acts as delivery vehicle for cholesterol. HDL picks up excess cholesterol and transports it back to the liver.

For decades there was a hypothesis that cardiovascular disease was caused by saturated fat and cholesterol accumulating along the walls of arteries. Since LDL delivers cholesterol it was labeled “bad” and HDL was labeled “good” because it collects cholesterol. 

The understanding of cardiovascular disease has improved considerably along with the ability to identify the different types and concentrations of lipoproteins in circulation.
LDL can further be divided into two types, large buoyant particles and small dense particles. Blood samples can be measured to see if there is a larger percentage of large buoyant LDL (pattern A) or a larger percentage of small dense LDL (pattern B). 

Despite the attention total cholesterol and total LDL has received over the last 60 years, they were never good indicators of risk from cardiovascular disease. There were frequent cases of serious cardiovascular disease in individuals with low total cholesterol.

It turns out the concentration of small dense LDL (pattern B) and the potential of small dense LDL particles to get trapped in arterial walls and then oxidize is a much stronger predictor of cardiovascular disease risk.

The U.S. Government Position on Fat

The Institute of Medicine (IOM) establishes Estimated Average Requirement (EAR), Recommended Dietary Allowance (RDA), Adequate Intake (AI), and Tolerable Upper Limits (UL) for nutrients. A consolidated list of their values was published in a 2006 Reference Manual (link below). 

The IOM found insufficient data to establish an EAR for total fat, so instead estimated an Acceptable Macronutrient Distribution Range (AMDR) for total fat of 20-35% of calories.

The 2006 IOM guidance on saturated fat is a good synopsis of what the U.S. Government position has been since the 1960’s:

“Saturated fatty acids can be synthesized by the body, where they perform structural and metabolic functions. Neither an EAR (and thus an RDA) nor an AI was set for saturated fatty acids because they are not essential (meaning that they can be synthesized by the body) and have no known role in preventing chronic disease. There is a positive linear trend between saturated fatty acid intake and total and low density lipoprotein (LDL) cholesterol levels and an increased risk of coronary heart disease (CHD). However, a UL was not set for saturated fatty acids because any incremental increase in intake increases the risk of CHD. It is recommended that individuals maintain their saturated fatty acid consumption as low as possible, while consuming a nutritionally adequate diet.”

There are no studies linking saturated fat consumption to CVD or CHD. The link between saturated fat and cardiovascular disease was a hypothesis which was never proven.

Credit Suisse Research Institute published an independent report on fat this year and stated:

“Plenty of research funding has been earmarked to study and back this hypothesis, yet we cannot find a single research paper written in the last ten years that supports this conclusion. On the contrary, we can find at least 20 studies that dismiss this hypothesis.”

The other maximal standards the DGAC based their findings on are the 2013 American Heart Association (AHA) Lifestyle Guidelines and a research review conducted by the DGAC looking specifically at fat consumption and hard outcomes (myocardial infarction, stroke, heart failure, and CVD related death). 

Hard outcomes were not looked at by the AHA Lifestyle Work Group. The Work Group focused on the impact of dietary patterns on Blood Pressure and Blood Cholesterol (focusing mainly on the impact to total Cholesterol and LDL). From the guidelines:

“The Work Group focused on CVD risk factors to provide a free-standing Lifestyle document and to inform the Blood Cholesterol guideline and the hypertension panel. It also recognized that RCTs examining the effects on hard outcomes (myocardial infarction, stroke, heart failure, and CVD related death) are difficult if not  impossible to conduct for a number of reasons (e.g., long-term adherence to dietary changes). However, the Work Group also supplemented this evidence on risk factors with observational data on hard outcomes for sodium. The Work Group prioritized topics for the evidence review and was unable to review the evidence on hard outcomes for dietary patterns or physical activity.”

The last line is significant. The 2013 AHA dietary review did not look at the relationship between dietary patterns and heart disease. It looked at the relationship between diet and LDL with the assumption that total LDL is an accurate predictor of heart disease risk (which it is not). 

There are two significant recommendations for saturated fat in the AHA guidelines:

• “Aim for a dietary pattern that achieves 5% to 6% of calories from saturated fat.” 

• “Reduce percent of calories from saturated fat.” 

Those two recommendations are significant because there are no traditional diets which follow those guidelines and the evidence supporting the recommendations is astonishingly thin. 

Thin Slice of Evidence 

Of the 6084 possible citations revealed in the initial search by the AHA Lifestyle Work Group for the question of diet, 28 articles discussing 17 studies were selected. 

The rationale for the first recommendation is listed under Evidence Statement 11 (ES11). ES 11 is based on three studies, DASH, DASH-Sodium and DELTA and from the AHA Lifestyle Report:

“Of note, in the DASH trials, the effect of saturated fat on LDL-C could not be isolated because macronutrients and other nutrients such as dietary cholesterol were not held constant.  In the DELTA trial, the dietary cholesterol and protein were held constant but other nutrients,including total fat and carbohydrates, differed in the comparison groups as shown in Table 4.  The LDL-C lowering is consistent in the DASH trials with the lower saturated fat dietary pattern resulting in lower LDL-C.  In DELTA, the greater reduction in saturated fat led to greater LDL-C lowering. “

Again, it is important to point out LDL is a poor indicator of heart disease risk. Lowering LDL-C does not mean the risk of cardiovascular disease is being lowered.

The second recommendation is also based on ES11 and adds ES12 and ES 13.

 Rationale for ES12 & ES13 is based on two studies done 11 years apart by the same authors. The results of their studies were based on computer predictions of effects (emphasis added):

“We used two meta-analyses from the same authors published 11 years apart in which they used the same inclusion/exclusion criteria and generated predictive equations to estimate changes in plasma lipids when substituting dietary fat types with carbohydrates or other fat types.”

It is worth pointing out the two AHA recommendations on saturated fat both carry the highest “Level I / Class A”rating: 

Level 1: Benefits >>>Risk. Procedure / Treatment SHOULD be performed / administered.

Class A:  Multiple populations evaluated. Data derived from multiple randomized clinical trials or meta-analyses. 

As stated above, “Aim for a dietary pattern that achieves 5% to 6% of calories from saturated fat.” is based on the result of one trial, DELTA and a lowering of total LDL. There was insufficient data to draw conclusions on the impact of saturated fat in the DASH trials. 

“Reduce percent of calories from saturated fat.” Carries a top rating despite the fact it is only supported by one trial (DELTA) and one set of researchers who did two computer prediction studies. 

Saturated Fat and CVD Risk

The 2015 DGAC also took a look at studies which examined links between saturated fat and cardiovascular disease endpoints. Seven meta-analyses were cited. None cited a link between saturated fat and cardiovascular disease. 

Four meta-analyses (Hooper et al.’s 2012, Mozaffarian et al., 2010, Farvid et al., 2014, Jacobsen et al.’s 2009 ) predicted a reduction of cardiovascular disease risk by replacing saturated fatty acids with polyunsaturated fatty acids.

From the DGAC Report on Hooper:

“there was no clear evidence of reductions in any individual outcome (total or non-fatal myocardial infarction, stroke, cancer deaths or diagnoses, diabetes diagnoses), nor was there any evidence that trials of reduced or modified SFA reduced cardiovascular mortality.”

Despite the lack of evidence one sentence earlier, the DGAC still reached the conclusion:

“These results suggest that modifying dietary fat by replacing some saturated (animal) fats with plant oils and unsaturated spreads may reduce risk of heart and vascular disease.”

Shortfalls in the Mozaffarian, Farvid, Jacobsen analyses are all covered in the Credit Suisse Report ‘Fat: The New Health Paradigm’. (Pgs. 37-39). 

References

2015 Scientific Report of the Dietary Guidelines Advisory Council
http://1.usa.gov/1MK8dQu

2015 DGAC Scientific Report Appendix E-2
http://1.usa.gov/1OuHklD

AHA – 2013 Lifestyle Guidelines 
http://bit.ly/1KS1UeH

AHA – 2013 Lifestyle Guidelines Full Workgroup Report
http://bit.ly/1KS2EAA

Credit Suisse. Fat: The New Health Paradigm
http://bit.ly/1KwjnFD

Alice Lichtenstein March 2014 NY Times Op-Ed
http://nyti.ms/1KS1K75

Institute of Medicine 2006 Fat Guidance
http://1.usa.gov/1MK8TW1

On Thursday, September 17th, The Credit Suisse Research Institute released the results of a one year study of dietary fat.

The report is a wealth of information.  I’d like to highlight three findings which you will hear a lot about in the coming months:

1) There is no link between consumption of saturated fat and obesity. A combination of sugar and solvent-extracted vegetable oils (canola, soybean oil, corn oil, sunflower oil, cottonseed oil, etc.) are the most likely cause of the current obesity epidemic. Over the past 50 years, vegetable oil consumption has increased by 89%.

2) “Doctors and patients’ focus on “bad” and “good” cholesterol is superficial at best and most likely misleading”. Total cholesterol and total LDL cholesterol are poor, if not dangerous measures of risk from cardiovascular disease. LDL particle size (a characterization of the density and size of cholesterol carriers) and a ratio of triglycerides to HDL has been found in clinical practice to be a much better indicator of CVD risk. 

3) The findings of the report are directly opposed to the latest recommendations found in the 2015 Scientific Report of the Dietary Guidelines Advisory Committee (DGAC).  The 2015 DGAC Report recommends reducing dietary fat below 10% and replacing saturated fat with Polyunsaturated Fatty Acids (PUFAs), primarily from vegetable oils. The Credit Suisse report finds fat consumption was 26% of total calories in 2011 and “if anything could increase safely well beyond current levels.”.  The DGAC recommendation is based solely on a handful of studies linking increased consumption of vegetable to a lowering of total LDL. There is no dispute that increased consumption of vegetable oil can lower LDL and total cholesterol. However, as stated above, total LDL has been shown to be a poor, if not dangerous indicator to use for assessing CVD risk.  The Credit Suisse report is well researched and based on a much wider and solid foundation.

The Credit Suisse report is outstanding and has significant implications for food manufactures, medical practitioners, health insurers and pharmaceutical companies. While there is still a lot to be learned about dietary fat, most of the confusion regarding nutrition revolves around fat and cholesterol and most of the confusion with fat and cholesterol revolves around an understanding of the effects of saturated fat, polyunsaturated fat and cholesterol on obesity and heart disease. The Credit Suisse report gets the relevant information out to a wider audience for sorting out. 

A copy of the report can be found here: Fat: The New Health Paradigm 

Strength

Christopher Sommers
Robb Wolf – Episode 213 http://bit.ly/1NCH97w
Robb Wolf – Episode 230 http://bit.ly/1NMTwMm
Robb Wolf – Episode 241 http://bit.ly/1NMTDaI
Robb Wolf – Episode 275 http://bit.ly/1NMTP9V

Pavel Tsatsouline
Tim Ferriss – Episode 55 & 57 http://bit.ly/1NMTYdu

Charles Poliquin
Tim Ferris – Episode ?? http://bit.ly/1NMUbNP

Fred Hatfield (Dr Squat)
Robb Wolf – Episode 261 http://bit.ly/1NMUlVe

Fuel

Dr. Peter Attia
Tim Ferriss – Episode 50 & 65 http://bit.ly/1U2STlk

Definitions:

Traditional Diets. Diets evolved from available plants and animals.

Industrial Diets. Diets constructed from individual macronutrients (protein, fat, carbs) and micronutrients (vitamins and minerals).

Links:
Diet, Intelligence and Longevity
HILLARD KAPLAN, KIM HILL, JANE LANCASTER, A. MAGDALENA HURTADO

How common are religious fasting customs?
What foods were banned?
How long did the fasts last?
What are the health implications?

Greek Orthodox Fasting Calendar

Muslim Fasting Calendar (Ramadan)

Jewish Dietary Customs

Fitness is a measure of the body’s work capacity.

Three indicators to evaluate fitness: 
Strength. Endurance. Skill. 

Three levers for improving fitness:
Stress. Recovery. Food.

Strength

Strength can be divided into three characteristics: capacity, alignment and mobility. 

Capacity is the measure usually associated with strength and is usually associated soley with muscles, ‘how much can you bench?’. A more nuanced approach I learned from Coach Christopher Sommers is to recognize there are three components to strength: bones, tendons and muscles and they all have different stress and recovery timelines.

Alignment is positioning. Bones are held in position by tension in muscles and tendons. Proper alignment maximizes power output and requires balanced tension. Posture is the most visible indicator of alignment.

Mobility is range of motion. To optimize fitness, mobility requires a balance between flexibility and tension. Hypermobility reduces work capacity and increases the possibility of injury. Limited range of motion reduces work capacity and increases the possibility of injury.

Endurance

Endurance is determined by the bodies ability to store, release and burn fuel. For simplicity, fuel can be divided into three categories: sugar, fat and blends. 

Anaerobic (absence of oxygen) endurance is fueled by glycogen (sugar) stored in the muscle. Effort at levels above the heart’s ability to supply blood with fresh oxygen are generally limited to two minutes or less. When anaerobic endurance thresholds are exceeded, muscles begin to shut down from acidosis (build up of hydrogen ions).

Aerobic (with oxygen) endurance is fueled by fat. The average body can be fueled by fat for well over a month (45 – 60+ days as a rough estimate).

Most exercise is fueled by a blend of sugar and fat with the proportion determined by the amount of oxygen available. For the average person at 65% VO2 max, a 50/50 blend of sugar and fat are burned with the sugar provided by triglycerides stored in tissue and glycogen stored in the liver. ‘The Wall’ in marathons or ‘bonking’ is primarily a result of depleting glycogen stores in the body. In a fasted state (ketosis), the body burns a blend of fat and ketones manufactured from fat by the liver to conserve sugar.

Metabolic chemistry is more complicated and involves other means of producing ATP (fuel), but characterizing the duration of effort (< 10 sec < 2:00 min < 4 hours) and the amount of effort (% of max heart rate) is a good way to develop a training and fueling strategy.

Skills

Skills consists of cues and direction of applied force. Skill is the demonstration of coordination. Coordination consists of muscles fired by cues from the senses. Said a different way, coordination is the right muscles fired by the right cues to generate force in the right direction. 

Stress & Recovery For Fitness

Fitness is different than health. At elite levels of athletics, health is often compromised to increase fitness. For the military and first responders, optimum fitness is often a higher necessity for survival than optimum health (longevity).
Although the goals are different, the same stress & recovery loads (physical, mental and emotional) are useful for prioritizing training.
The type, quantity and duration of load and recovery are adjusted to make specific impacts on the strength, endurance and skill indicators listed above.

The indicators listed above provide higher fidelity on where work capacity (fitness) can be improved. 

Food For Fitness

Like stress and recovery, food can also be used as a lever for improving fitness but the intent is different.

The quantity and sources of sugar and fat in the diet will directly effect body composition and the ability of the body to store, release and burn fuel.

While ingredients from plants and animals can easily provide all the required nutrients for an average person, high work outputs may require concentrated supplements with the associated risk of toxicity.