4 May 2016

WTC7 - A New Risk in Operational Firefighting?

Let’s first define why this is so important. In terms of political history, this is probably the most important building collapse ever to have occurred; not just from an architectural perspective, not only because it raises very significant questions about the safety of high-rise occupiers and their rescuers should a similar building be involved in fire but because of what it represents in terms of what happened geopolitically and militarily as a result of its collapse. However, the primary purpose of this assessment is to establish what level of risk the report of this collapse identifies for Firefighters.

Short introductory film :-




Summary of Findings

   The building was modern, in good condition, steel-framed with reinforced concrete floors, with high-specification class-A fire protection (2-3 hours’ fire-protection-rated and easily able to tolerate normal fires).

   Extensive damage was caused to the south face from falling debris, but the NIST report states that this was not a contributing factor in causing the building’s collapse. Engineers have demonstrated that if this damage were to be considered a major factor the building would have fallen asymmetrically, toppling in the direction of that damage.

    There is suspicion about what ignited the fires and when they started. NIST reports falling debris as a “likely” cause from the north tower collapsing at 10:28am, however, there were witness reports of “thick smoke” and an explosion from within Building 7 at about 9:30am which contradicts this claim.

   The fires were normal in size, the sort of fires to be expected in any normal office type environment. There was nothing extraordinary about their fuel source or location that might explain a prevention of effective fire-fighting operations.

    The building’s fire alarm was linked to the automatic sprinkler system. The fire alarm had been deactivated due to being set in test mode for 8 hours that day, starting at 6:47am, it failed to reactivate at 2:47pm.

    The sprinklers did not activate. The official report claims that the sprinklers did not activate due to a broken water main. There is strong evidence to support good mains water supplies, which could have been supplemented and boosted by a manually operated sprinkler system pump in the building.

    The sprinkler system could also have been charged by FDNY from external siamese fittings outside the building. This did not happen.

    Firefighting operations were prematurely curtailed in Building 7. Firefighters were withdrawn from the building early in the day based upon the orders of an unknown city official who predicted the unprecedented fire-induced collapse of this building 5 hours in advance.

    The official reasons provided for the Firefighters’ withdrawal included an alleged lack of water and resources. Water was available in ample volume via the city water mains, and from 3 fire boats located nearby on the river Hudson, each capable of providing up to 18,000 gallons of water per minute. Fire-fighting resources in lower Manhattan were at an all-time high. There were more fire-fighting resources, including, in the face of terrible and unprecedented FDNY loss of life, an army of very willing and eager Firefighters wanting to work.

   The official study and technical theory of the collapse of the building are, according to thousands of architects and engineers, unscientific and false. These same engineers and architects are endorsed by scientists who confirm that the NIST explanation is not only false but impossible.

    NIST refuses to release its data for peer-review and has routinely refused to answer difficult questions from experts about inconsistencies and errors in its theory of collapse.

    When the building collapsed there were many witnesses reporting the sounds of loud, fast and repeated explosions. Military grade nano thermite residues were discovered in the dust of the remains of the buildings. This fact has been confirmed via an independent and international rigorous scientific peer review process.


   When the building did collapse it fell at a scientifically verified rate of acceleration indistinguishable from free fall. This is of great significance and importance. For a large building (100 metres side to side) to collapse with a level roof line, the building’s entire structural integrity must have been removed simultaneously and almost instantaneously.

   In NIST’s August 2008 Draft Report the building’s free fall was denied. The lead investigator at NIST had openly dismissed free fall having occurred, correctly stating that this fact would require zero structural integrity in the building.

   Due to the intervention of a high-school physics teacher, in the November 2008 Final Report NIST was forced to admit that free fall occurred, but they understated its significance in the report and totally avoided elaborating upon the aforementioned implications of what it identified.

    There is only one explanation for the nearly instantaneous and simultaneous removal of the building’s entire structural integrity which caused its free falling collapse - controlled demolition.

   The collapse of this building exemplified seven features of a textbook description of a controlled implosion:

1.    The collapse started from the bottom.
2.    The onset of the collapse was sudden.
3.    The collapse was total.
4.    The building came straight down.
5.    Its acceleration approximated that of a free-falling object.
6.    Most of its concrete was pulverized into tiny dust particles.
7.    The building ended up as a relatively small pile of debris.

   Professional controlled demolition experts agree that Building 7 must have been collapsed by controlled demolition, with the added affirmation that this sort of collapse is not possible due to fire alone.

   Based on the fact that a steel-framed building has never before in history collapsed due to fire, the accurate and certain foreknowledge of the collapse 5 hours before it occurred, based only on alleged noises coming from within the building, is extremely questionable, to say the least. The only feasible explanation for this level of certain foreknowledge, which was shared with many emergency workers in the area without explanation, is that this information was based on action based foreknowledge. Complete building collapse due to fires is unprecedented, those who accurately predicted the collapse 5 hours in advance must have known actions had been taken to cause the collapse to occur when it did.
  • Researching NIST’s credibility has revealed a very broken scientific reputation. It is an agency of the US Department of Commerce. During the years it was writing its World Trade Centre reports, it was, therefore, an agency of the Bush-Cheney administration. In 2004, the Union of Concerned Scientists published a document charging this administration with “distortion of scientific knowledge for partisan political ends.” By the end of the Bush administration, this document had been signed by over 15,000 scientists, including 52 Nobel Laureates and 63 recipients of the National Medal of Science.
Conclusion
Since these events 15 years ago, Firefighters' operational procedures have not been changed for fighting high-rise fires. In the UK, local government 'Stay put' policies, which advise residents in high-rise buildings and flats to remain in their property when there is a fire, have not been modified. The building design regulations have not changed and equivalent buildings have not been retrofitted with modifications to prevent a recurrence of Building 7's collapse.

However, if NIST's official report of what happened to Building 7 is maintained by our authorities as a valid explanation of events, in accordance with the Health and Safety at Work Act and other related legislation, all of the above factors need to be questioned and critically reassessed as a matter of great importance by fire services, local housing authorities, and building standards regulators.

Generally, as a rule, we tend to rely upon science rather than unfounded belief to understand our world.  Science is defined as the search for truth. When a scientific truth is found, fundamentally this is always based upon a preponderance of positive probabilities.  We hold these findings as true until we find a good reason to believe otherwise.  A true and honest scientist will always accept questioning of his hypothesis and continue to test its validity. From my observations of NIST’s analysis of this collapse, observations shared by many highly qualified professionals in their respective fields, an honest scientific approach has not been pursued.

The deliberate and immediate removal and destruction of nearly all the evidence at the scene of the crime, the failure to even mention the collapse of Building 7 in the 9/11 Commission Report, combined with the catalogue of errors and omissions in the NIST report, all aggregate to destroy any credibility the report might hope to convey.
The claims made by NIST that the sprinkler operation and fire-fighting efforts failed, due to poor water supplies and limited resources, were false and only serve to further diminish their credibility. This building’s fires could have been contained and extinguished well in advance of the alleged structural failures.

The experts' evidence of the building's uninhibited gravitational free fall acceleration, its symmetrical collapse perfectly into its own footprint, witness testimonials of explosions, evidence of explosive residues, and 'certain foreknowledge' of the building’s collapse, all points compellingly towards an alternative hypothesis - a deliberate case of controlled demolition. A hypothesis which, if the scientific principle of Occam’s razor had been applied, should have been the first to have been tested.

This analysis has been completed without being influenced or prejudiced by the details of the politics in the background of this incident. The data and the evidence alone dictated what the study discovered. Unfortunately, it’s an unavoidable fact that this case is connected with politics and, speaking personally, I can say with open sincerity that I trust Newtonian Physics and the laws of nature infinitely more than I trust politics. As previously stated, gravity is not just a good idea, it’s a law. In agreement with thousands of expert architects, engineers, and scientists, the findings of this analysis identify that the risks to Firefighters at this incident were not due to faulty architecture, sub-standard engineering, untested fire-fighting procedures or a miraculous fire-induced building demolition.

The sudden and complete collapse of a steel-framed high-rise building due to normal fires presents as little risk to operational Firefighters today as it did in the days before this event. 




*****************
In an attempt to expose this evidence and demand an independent re-investigation thousands of Architects and Structural Engineers across America are campaigning to reveal the truth of the above and more. You can find their excellent website at www.ae911truth.org

Additional recommended viewing:-


A collaboration between US Firefighters and Architects presentation:-





Excellent presentation detailing the extent of foreknowledge by the BBC, CNN, and some of the FDNY identifying that WTC7 was certain to collapse:-




Technical details of problems with the NIST hypothesis, including details of omissions proven from FOIA requests:



Excellent talk of the physics of the building 'collapses':

11 Apr 2013

Unhealthy Saturated Fat - What is the reality?

I dedicate this post to a friend who looks at me like I'm a two-headed alien when he hears me saying that saturated fats are perfectly healthy. And who can blame him! I completely understand why he, or any normal person, would think this way.  To believe that saturated fats are healthy goes completely against all conventional wisdom. 

Up until about five years ago I also believed saturated fats were very unhealthy and strongly linked to heart disease and other illnesses.  These beliefs were based upon the information I had grown up with, as well as some of my University education in the 90's which scratched the surface of the pathophysiology of heart disease.

Even today in 2013 one of the most common misconceptions regarding nutrition is the fear of cholesterol and saturated fats.  This stems from their long-standing mislead association with ischemic heart disease.  Where does this misconception originate?

The common fear follows this pattern of logic: When you eat foods high in saturated fats, the fat and cholesterol in these foods enter your blood, become all gloopy and stick to the inside of your arteries.  

At a very simplistic level, the assumption is made that because these saturated fats are solid outside the body, they will solidify inside your bloodstream too; and even though the internal average temperature of a human being is significantly higher than room temperature, the arteries much like simple non-biological plumbing waste pipes get caked up with hardened fat, blood flow is restricted, and a wham - heart attack!

The above sounds so over-simplified that you'd immediately think "Who'd be gullible enough to believe that?!".  Most Brits might because its what they've been told by the British Food Standards Agency.  In 2009 the following TV advert was broadcast in the UK by the FSA.  They used that very same metaphorical description to perpetuate the fear of saturated fat. Why? Because they're as confused as everyone else, and it's easier to sell a simple lie, than to fathom or explain a more complicated truth.




None of the prominent scientists who originally promoted the idea that cholesterol might be a factor in the development of heart disease ever believed anything remotely resembling the above nonsense. 


A deeper understanding of the pathophysiology of coronary heart disease reveals that whilst cholesterol is indeed found in the plaque which builds up in the arteries which supply the heart muscles with blood, it's a gross over-simplification to conclude from this that cholesterol itself must therefore be the cause.

In research dating back to the turn of the last century, scientists recognized the complex nature of how atherosclerotic plaque accumulates not on but behind the layer of the artery in contact with the blood, called the endothelium, and that the cholesterol and fat within it is engulfed in white blood cells as part of an inflammatory process.


The truth is that there is no real correlation between cholesterol levels and cardiovascular disease, not by age groups, not by gender, and not by population.  But don't take my word for it, start by watching the following very short video by Dr Malcolm Kendrick:



The nutritional advice that our government, National Health Service, and most mainstream nutritionists has been providing us regarding saturated fats and cholesterol is unfortunately based upon fundamentally flawed principles.  The mainstream dogma is so seriously off target, that excellent, free-thinking, and well-read Doctors are starting to stand up and demonstrate their dissatisfaction.



The cholesterol precept is so entrenched in mainstream medicine that an organisation called The International Network of Cholesterol Skeptics (THINCS), made up of many leading doctors in the field from around the world, is trying to change the views of the medical community in this area.  As a result more and more Doctors are becoming aware of the weaknesses in the research which formed the foundation of what they were taught at med-school.



The misunderstandings regarding saturated fats and cholesterol have many origins, but can primarily be traced back to over-simplified misrepresentations of research drawn from the cholesterol-fed rabbit and the pathology of the genetic disorder - familial hypercholesterolemia.  

Nikolai Anichkov's 1913 cholesterol-fed rabbit model, which is where much of the confusion started, was predominantly viewed as a model of hypercholesterolemia, but it revealed much more than this.  It also identified the crucial role of lipoproteins, their oxidation, and the importance of healthy clearance of unstable lipoprotein lipids from the bloodstream. 



Nikolai Anichkov's 1913 cholesterol-fed rabbit model, simplified pictorially above, was a model not merely of hypercholesterolemia but of hyper-oxidized-lipoproteinemia.








The saturated fat  and cholesterol misconceptions were perpetuated further in the 1950s by the selective research findings of an American biochemist named Dr.Ancel Keys.  Among his most famous research is the "Seven Countries Study" - probably the most notorious example of falsified research in the field of nutrition. 




The American government bought into Keys' hypothesis and the rest of the west followed.  As a result many western government health departments, the media and the medical-pharmaceutical complex have demonized saturated fats and cholesterol for decades.


The adverse effects of Ancel Keys' research upon health, quality of life and medical research are inestimable.  His scientific shenanigans were borne out of a need to be right, at the expense of honesty.  He had a pet hypothesis and was clearly blinded by his own bias and need to validate, not investigate. He cherry picked his data to support his pre-existing idea of the connection between saturated fat, cholesterol and heart disease. 

In a 1957 paper, Dr. Jacob Yerushalmy, founder of the biostatistics graduate program at the University of California at Berkeley, pointed out that while data from the six countries Keys examined seemed to support the diet-heart hypothesis, as mentioned in the above clip,  statistics were actually available for twenty-two countries, but fifteen of these did not support Keys' pet hypothesis so he discarded them! (He also counted the UK as two countries, separating the data from England and Wales) 

When all 22 were analysed, the apparent link between fat consumption and heart disease disappeared. Further flaws in Keys' reports were identified by Dr. Raymond Reiser's research in 1973.

The other prominent criticism of Keys’s study was that he had observed only a correlation between two phenomena, not a clear causative link. This left open the possibility that something else was leading to heart disease, which is only now starting to become more apparent.



If saturophobes want more proof, search through the medical publications for research similar to  this meta-analysis which shows that over a 5-23 year follow-up of 347,747 subjects, there is no association between the intake of saturated fat and heart disease or stroke.  

A concise account of research supporting the health benefits of eating saturated fats and cholesterol is presented in David Evan's book "Cholesterol and Saturated Fat Prevent Heart Disease", which provides evidence from 101 scientific papers.

Much of the controversy and debate about cholesterol focuses on correlations with cholesterol.  What is their magnitude? How consistent are they? Why do they exist in the young but not in the old, and in men more than women?

The cholesterol debate really misses the point.  Since the early 1980s the molecular evidence has made it very obvious that it is oxidised Low-Density-Lipoprotein (oxLDL) that contributes to atherosclerosis, a situation which is highly exasperated by polyunsaturated oils and minimised by saturated fats - as recently identified by this 2013 study.

Branding saturated fat as unhealthy is problematic because we need fat in our diets, and its displacement is resulting in its substitution with more harmful unsaturated fats and oils.  Any well intended advice recommending the avoidance of saturated fat is having the opposite effect and causing long-term harm.

The magnitude of the scientific debacle surrounding saturated fats is summed up nicely by nutritional biochemist Dr. G. Mann - "The Diet-Heart Hypothesis is the greatest deception of our times" (From -Coronary Heart Disease - "Doing the Wrong Things" )

Other saturated fat related articles:-


10 Apr 2013

Increasing PUFAs while reducing SFAs increases mortality rates


Increasing dietary polyunsaturated fats and decreasing saturated fats is associated with an increase in both overall death rates and heart disease death rates
Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.
Source
Laboratory of Membrane Biophysics and Biochemistry, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA. Chris.Ramsden@nih.gov
Erratum in
·         BMJ. 2013;346:f903.
Abstract
OBJECTIVE:
To evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death.
DESIGN:
Evaluation of recovered data from the Sydney Diet Heart Study, a single blinded, parallel group, randomized controlled trial conducted in 1966-73; and an updated meta-analysis including these previously missing data.
SETTING:
Ambulatory, coronary care clinic in Sydney, Australia.
PARTICIPANTS:
458 men aged 30-59 years with a recent coronary event.
INTERVENTIONS:
Replacement of dietary saturated fats (from animal fats, common margarines, and shortenings) with omega 6 linoleic acid (from safflower oil and safflower oil polyunsaturated margarine). Controls received no specific dietary instruction or study foods. All non-dietary aspects were designed to be equivalent in both groups.
OUTCOME MEASURES:
All cause mortality (primary outcome), cardiovascular mortality, and mortality from coronary heart disease (secondary outcomes). We used an intention to treat, survival analysis approach to compare mortality outcomes by group.
RESULTS:
The intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6% v 11.8%, hazard ratio 1.62 (95% confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2% v 11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3% v 10.1%, 1.74 (1.04 to 2.92), P=0.04). Inclusion of these recovered data in an updated meta-analysis of linoleic acid intervention trials showed non-significant trends toward increased risks of death from coronary heart disease (hazard ratio 1.33 (0.99 to 1.79); P=0.06) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07).
CONCLUSIONS:
Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.
TRIAL REGISTRATION:
Clinical trials NCT01621087.

6 Feb 2013

Cardiovascular Damage from Extreme Endurance Exercise

As someone who has exercised to the extremes all my life, the following video is very sobering whilst honestly not too surprising.  Your heart is like any other organ in your body, it gets tired and will show the effects of years of over-use to your detriment if it's asked to do too much, too often.

22 Nov 2011

The Israeli Paradox


Diet and disease--the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet.

Source

Department of Membrane Research and Biophysics, Weizmann Institute of Science, Rehovot, Israel.

Abstract

Israel has one of the highest dietary polyunsaturated/saturated fat ratios in the world; the consumption of omega-6 polyunsaturated fatty acids (PUFA) is about 8% higher than in the USA, and 10-12% higher than in most European countries. In fact, Israeli Jews may be regarded as a population-based dietary experiment of the effect of a high omega-6 PUFA diet, a diet that until recently was widely recommended. Despite such national habits, there is paradoxically a high prevalence of cardiovascular diseases, hypertension, non-insulin-dependent diabetes mellitus and obesity-all diseases that are associated with hyperinsulinemia (HI) and insulin resistance (IR), and grouped together as the insulin resistance syndrome or syndrome X. There is also an increased cancer incidence and mortality rate, especially in women, compared with western countries. Studies suggest that high omega-6 linoleic acid consumption might aggravate HI and IR, in addition to being a substrate for lipid peroxidation and free radical formation. Thus, rather than being beneficial, high omega-6 PUFA diets may have some long-term side effects, within the cluster of hyperinsulinemia, atherosclerosis and tumorigenesis.

18 Mar 2011

Understanding Body Fat


Having a good understanding of the actual physiology of body fat regulation, including how fat enters the body, how it is created within the body, how it gets stored, how you mobilise it, the best way to maximise its use, whilst minimising its storage above and beyond desirable levels, will put you one step ahead in your quest to control body fat. 
The progress of a fattening adipocyte
In order to maintain strength and survive times when food was not easily available, your body needed a clever, space-efficient way to store and carry plentiful supplies of energy.  We have a beautiful and ingenious solution to this physiological problem, it's called adipose tissue or body fat!


In the past, body fat was fundamental to survival and a highly desirable attribute.  Today you might think differently.  You possibly even hate your body fat, however your body and particularly your genetic blueprint is stuck in the past, and it loves your fat.  The body thinks your fat is so fantastic that if your fat stores become significantly threatened it will take very effective steps to protect them.


Fat is space efficient, easy to store, doesn't use much energy to sustain, can store an almost unlimited amount of calories; and if your fat cells do get full, your body will simply make new ones to store even more incoming calories.

Controlling your body fat levels may not appear to be the most complicated of sciences.  Ask most people how to lose fat and you'll usually get the simplistic answer: eat less and move more!  To a certain extent at a simplistic level this advice works, at least within a certain range of body fat percentages.  That is, the higher one's body fat levels are the more willing those fat stores are to relinquish their fatty acids for use as energy; whereas when at lower body fat levels, fat tissues become reluctant to part with their fat, becoming resistant or stubborn. 

As complex biological systems we do not strictly operate in compliance with the basic principles of physics.  The human body is not a closed system and the many mechanisms which regulate its vital functions, including body fat regulation, change continually depending upon multiple inter-related factors.

Fundamentally, if you create a calorie deficit where less energy is consumed than your body needs to meet the sum of its basal energy requirements, plus its activity requirements, then you should tap into and burn off your fat stores.

Some nutritional authors claim that the above is a misleading over-simplification of the problem.  To a degree they have a point as poor dietary composition will make fat loss slower and more difficult, and the type of exercise used to accentuate fat loss can have dramatically varying results.

However it has to be said that regardless of which ever route one does take there is no escaping the fact that calorie balance, or more precisely imbalance, is critical!  There is no such thing as an eat all you want fat-loss diet, unless the composition of the diet causes you to want less, and in turn you eat less calories than your body actually burns, either due to physiological effects such as ketone and NEFA suppression of appetite, or because a diet is simply so unpalatable that you choose not to eat much!

It is also misleading of some researchers to suggest that exercise is not a worthwhile tool in the regulation of body fat and as a treatment for obesity.  It is true that good exercise will always struggle to fix the metabolic problems caused by a poor diet, unless the diet is improved.  A balanced and intelligent exercise regime, tailored to individual needs, combined with an intelligent diet will synergistically and powerfully accentuate fat-loss. 

Some of the complications which compound the theories of calorie balance are evident when considering the concept of partitioning. For some introductory information to this read this short post - A Basic Introduction to Calorie Partitioning.

From a body fat management perspective, what we are really interested in, more so than just a calorie deficit, is a fat deficit.  Essentially to lose body fat you need to create a fat deficit. This means that you must be burning more fat than your body is consuming or creating.  To maximise fat loss you need to optimise this process.

Some genetically gifted people, the sort who can eat whatever they like and never gain a pound, are able to easily access and use their body fat more effectively than most normal people, even when eating a standard mixed diet with plenty of carbohydrates. This most likely occurs because they have an excellent natural ability to partition different types of fuel.  They are able to continue burning fats when glucose is freely available but is needed to replenish the body’s glycogen stores, and they efficiently use glucose as a primary fuel without rushing it into fat stores when its supply dominates. They are also likely to have favorable body fat distribution, with less stubborn fat, and probably less fat cells in general.

Unfortunately for them this genetic luck doesn’t always correlate with good health, nor does it tend to last forever.  Usually when they reach their late thirties and beyond, their physiology can become resistant, glucose management starts to falter, and the fat starts to show.  Having a tendency to shunt excess carbohydrates into fat storage via efficient fat tissue de novo lipogenesis may actually help protect individuals from the chronic ravages of high blood glucose levels over the years.

With the right kinds of dietary modification and exercise, you can significantly improve your partitioning ability so that your body will eagerly conserve glucose and proteins, whilst preferentially burning fats for fuel, thus making your regulation of body fat less of an up-hill struggle.

Dietary fat

Let's start with dietary fat, the fat that's found in your food.  All dietary fat is technically packaged as a triglyceride, which is a glycerol molecule bound to three fatty acids.  These fatty acids come in various different sizes and types, with chemical differences which can impact upon physiology, metabolism, and health. They can vary in length from short to long chain, with corresponding numbers of carbon atoms. They also vary in their degree of saturation, which is determined by their number of double bonds.  Saturated fats have no double bonds, monounsaturated fats have a single double bond, and polyunsaturated fats have multiple double bonds. 

When digested and absorbed in the intestines, fats are packaged into lipoproteins called chylomicrons, and transported via the lymphatic system into the bloodstream.  For more detail on this process see my article entitled “Lipoprotein Physiology”.

A number of hours after eating, these chylomicrons will reach the various target tissues; including muscles, the heart, adipose, and the liver. The tissues which need fats to burn as fuel, or to replenish their fat stores, express an enzyme called lipoprotein lipase (LPL) which draws the fatty acids from the chylomicron.

The fate of these fatty acids when they reach these tissues depends upon a number of factors determined by your current metabolic state.  Obviously, to reduce body fat levels we want all incoming fatty acids to be used or burned rather than stored, whilst ideally we also want stored body fat to be tapped into and burned.

Body fat

Body fat, like digested fats, is stored as a triglyceride inside fat cells in various types of fat tissue, as well as within the muscles, called intramuscular triglycerides.

Way back in 1965 Jules Hirsch observed that the fatty acid composition of body fat closely resembles that of the diet.  In trials he found that when subjects were given different controlled fatty acid compositions in their diet for sufficient time to allow for whole adipose turnover, their adipose fatty acid composition changed to closely resemble that of the dietary fatty acid composition. 

An average sized person will have somewhere in the region of 25-30 billion fat cells which are composed of about 90% triglyceride, with the remaining 10% being water and the enzymatic machinery which controls their cellular metabolism.

There are 5 main different types of body fat: essential, brown, visceral, intra-muscular and subcutaneous. 

Essential body fat

Essential body fat; in the brain, nervous system, and other tissues; accounts for about 5% of men’s body mass, and about 10% of women’s body mass.  It’s called essential because without it you wouldn’t be alive.  Women are genetically programmed to retain a higher minimum 'essential' level of adiposity to prepare them for pregnancy and lactation.  These differences underlie one of the main reasons why a women’s body fat percentage cannot, in the vast majority of cases, drop to the single digit levels that men can achieve.

Brown fat

Brown fat is a unique type of fat which actually oxidises the other types of fat to produce heat. In contrast to the other types of fat, which are primarily triglyceride, brown fat consists mainly of mitochondrial mass (the energy production reticulum of the cell), with very little triglyceride. This high mitochondrial density makes brown fat ideal for burning fatty acids for the creation of heat. Animals tend to have significant amounts of brown fat, which they use to generate heat.  

Until recently it was believed that humans did not retain their brown fat beyond infancy, which pretty much discounted it as a factor in adult body fat regulation.  However, from scans carried out to detect metabolic activity in tumours, it has recently become clear that some adults do indeed possess brown adipose tissue, predominantly around the neck and shoulder area, and that the metabolic activity of this tissue increases in response to exposure to cold.

Visceral fat

Visceral fat, also known as organ fat or intra-abdominal fat, is located inside the abdominal cavity, packed in between organs. An excess of visceral fat is known as central obesity as it creates a pregnant look, causing the abdomen to protrude. Excess visceral fat is linked to diabetes, insulin resistance, inflammatory diseases, and other obesity-related diseases.
Men tend to have more visceral fat than women as it tends to correlate with both testosterone and cortisol levels.  

Female sex hormones correlate with increased fat storage in the buttocks, thighs, and hips in women. When women reach menopause and their estrogen levels decline, fat migrates from their buttocks, hips and thighs to their waist.  

When researchers pump sex-change patients up with hormones, they see a shift in bodyfat: men take on female bodyfat patterns and vice versa.  Female athletes and body-builders who use anabolic steroids, or who have higher than normal testosterone levels, also tend to accumulate visceral fat.

When losing body fat, visceral fat is lost relatively easily compared with subcutaneous fat, so by the time men reach the 11-14% body fat range, it is unlikely that they will carry much visceral fat, unless they have been using steroids.

Because dieters are generally more aware and conscious of their subcutaneous fat levels, the preferential use of visceral fat before subcutaneous fat by the body in response to dieting can give the impression that the diet is failing to remove visible fat!  This occurs because visceral fat has a better blood supply, is more insulin-resistant, and has a greater sensitivity to adrenal fat-burning stimulation.  So when losing fat this is generally burned faster and more significantly than subcutaneous fat.  When the visceral fat drops to the lower levels mentioned above the contribution of subcutaneous fat to energy provision increases.  This is also when fat loss becomes much more dependent upon the right hormonal environment.

Intramuscular fat

Intramuscular fat is stored, as its name suggests, within muscles (predominantly next to the more aerobic fibre sub-types) as triglycerides (IMTG).  In a fatty cut of beef IMTG can be seen as the marbling in the meat.  

In humans eating a mixed diet, the excess accumulation of intramuscular fat is associated with insulin resistance and type-2 diabetes among the normal population. However, in fat adapted humans with low carbohydrate intakes, plentiful IMTG storage it is likely to be normal, healthy, and advantageous.

Endurance athletes often do not exhibit the insulin resistance associated with higher levels of IMTG.  They are typically insulin sensitive while having high levels of IMTG, due to their muscles’ trained ability to process both fats and carbohydrates.

Women have been shown to use more IMTG during exercise than men, which directly correlates to the higher IMTG content in women.

IMTG stores act as an energy buffer zone or intermediate energy reservoir, ensuring a consistent rate of supply of fatty acids commensurate with demand for their oxidation, at times when plasma free fatty acid levels may fluctuate in response to varying metabolic conditions.

Subcutaneous fat

This is the kind of fat we all love to hate!  Subcutaneous fat is found just below the skin in a region called the hypodermis. 

As mentioned earlier, due to hormonal differences, in men subcutaneous fat tends to accumulate around the midsection and low-back; whereas in women, it tends to be on the hips and thighs.  This hormonal influence is generally the reason for kids displaying different body fat accumulation patterns before and after puberty.

Not all subcutaneous fat appears to have been created equal!  It appears to exist along a continuum ranging from normal, to what has become termed as stubborn fat.  This can be very difficult for some people to lose.  It comes off last, if it ever comes off at all, and it’s generally stored where you want it the least – around the 6-pack and low back in men, and hips and thighs on women.

To fully appreciate the complexity of body fat one needs to be aware that rather than just being a simple and inert energy store, fat tissue is an element of the endocrine system, secreting powerful self-regulating hormones such as leptin, resistin, and also cytokines. 

To complicate matters further, the various different types of fat tissue behave differently in response to the fat mobilisation signals initiated by the brain and endocrine system.  The fat tissues possess different degrees of blood supply and insulin sensitivity; complicated even further by their specific type and distribution certain adrenoreceptors; which in turn are affected by thyroid hormones and testosterone levels.  The distribution and density of the enzyme lipoprotein lipase (LPL), which determines the rate of fat uptake of a fat cell and the pattern of fat distribution around the body, is also influenced hormonally. 

Fat also behaves differently in relation to a person's total fat mass, that is, the fatter someone is the more willing the fat tissue is to relinquish its stores, and vice versa.

The complexity of body fat regulation is apparent not only in our varied individual tolerance to carbohydrate intake and insulin responses to food, but also in the individual variability of our body fat's responsiveness to hormonal cues for both energy storage and energy liberation.

All these factors impact upon fat's behavior and response to various nutrition and exercise interventions, and highlight some of the potential short-comings of the energy balance paradigm.  In short, it is not advisable to view the human body like an abacus counting calories in versus calories out, whilst this approach works in a strictly controlled lock-down system ( see the Minnesota Starvation Experiment), it is difficult for most normal people to adhere to in normal life.  It is true that for a diet to be successful it needs a calorie deficit, but for sustainability it also needs to be holistic and consider the effects of various foods upon appetite, hunger drivers, psychology, nutrition, long-term health, and so on.

Personally, I have had success with diets at both ends of the spectrum.  As a triathlete training over 20 hours per week, I found a low-fat, high-carb diet effective, but this had to be monitored tightly with calorie recording.  High volumes of full-spectrum aerobic exercise will use a lot of carbohydrates, thus physiologically creating a consistent exercise induced low-carbohydrate state within the body, which in turn results in good use of fat stores during exercise and recovery.  Without lots of exercise the low-fat, high-carb system requires lots of self-discipline and a significant amount of hunger.

At the other end of the spectrum, I have had great success eating a ketogenic diet.  I found this most effective when exercising less, especially at non-competitive intensities.  Dietary induced fat-adaption, combined with intermittent fasting and regular low- to moderate-intensity aerobic exercise helps burn off fat stores very effectively, without feeling hungry all the time.  You will however need to be disciplined in your eating, as carbohydrates will be missed, and calories do still matter.  One also needs to be aware of the insulinogenic capacity of proteins, like beef for example.  For this reason I tend to reserve my protein intake for the evening meal.