intermittent fasting

Fasting and calorific restriction- Increased longevity or just a slower death?

Copy of Untitled Design.jpg

Intermittent fasting and calorific restriction (CR) seem to be the Zeitgeist of today’s nutrition and wellness sphere and has comparisons with the raw green sludge breakfast smoothie and these approaches to health. CR is often being touted as health enhancing because of a premise that sounds something like this. You fast or eat less than X calories and that has the capacity to slow down metabolism, ensuring that you produce less oxidative stress, autophagy ensues, and this opens up your 8th chakra ready for your beyond meat whopper. It’s true that fasting and CR can probably enhance your health when you are prone to over eating, and beyond that nothing else. Yes you will lose weight (seen as that’s the only variable that many people care about these days), but that result is down to one key fact. You are in a calorie deficit. Can you rebound from that restriction is the question that most need to evaluate.

CR and fasting promotes improvements to health and extending lifespan but the main reasons that it promotes longevity is probably for several reasons that include.

1. The restriction of polyunsaturated fats or PUFA.

2. The restriction of methionine, cysteine and sometimes tryptophan.

3. Perhaps less consumption of pesticides and metals.

The question of do you need to fast, should be rephrased with do you even need to fast? What about addressing what can extend lifespan and still maintain an optimal level of metabolism?

PUFA and mitochondrial uncoupling

Let’s start with PUFA which are commonly known as vegetable, seed, fish, soy and other oils, including olive oil (which is the better of the lot and when used cold has some useful qualities). The other oils share similarities, as they are all unstable especially so when heated. The most unstable oils in general use and over recommended are the omega 3’s particularly DHA and EPA. I’ve recently seen so called holistic practitioners recommending in excess of 6 grams of DHA to improve anti-inflammatory responses and so-called membrane fluidity. One of the key problems with this approach is that increased DHA levels are known to occur in the obese and diabetics (Madison Sullivan et al., 2018) and this increase is associated with reduced mitochondrial enzymes (metabolic enhancers).

 

PUFAs like DHA are often touted as protective because they induce a process called mitochondrial uncoupling. This can occur when your’e cold, when you don’t produce enough thyroid hormone and other stressors. It can indeed be protective but DHA for example creates something called proton leak within the cells, and decreases the efficiency of the cell. Oxygen efficiency is lost and production of energy or adenosine triphosphate (ATP) is also wasteful. This sits well with many who promote theoretical mechanisms of longevity such as the rate of living theory (Speakman et al., 2004) (Vaanholt, Daan, Schubert, & Visser, 2009) and the membrane pacemaker theory (Hulbert, 2007; Hulbert, Kelly, & Abbott, 2014). A. J Hulbert is a well-respected thyroid researcher who completed a large body of work on the role of thyroid hormones and fatty acids and their role in ‘membrane fluidity’. Interestingly Hulbert proposes that mammals and birds with a high metabolic rate (much like Elie Metchnikoff’s theories that link low gut bacteria with metabolism in birds, mammals and longevity) and increased longevity often have this key feature in common. They generally have low saturation of PUFAs as determined by something called the peroxidation index (PI). Conversely animals with high PUFA and PI have decreased longevity, but the membrane pacemaker theory postulates it as high metabolic rate, inducing uncoupling and characterized by increased reaction oxygen species (ROS) and the production of superoxide and superoxide dismutase (SOD).

hulbert membrane.jpg

“There’s an inverse relationship between the peroxidation index of skeletal muscle phospholipids and maximum lifespan of mammal and bird species of different sizes.” A.J.Hulbert

 

 This forms a major component of the rate of living theory or that increased metabolism generates ROS ergo slowing metabolism down, produces less ROS and that’s productive. Although it’s not and this is where many people get confused about efficient thyroid function, enhanced metabolism and potential oxidative stress. I was reminded by a Ray Peat Newsletter earlier on the year how SOD remains elevated throughout the lifespan of those with Down syndrome and that serotonin increases SOD, contributing to decreased longevity. With excess PUFA consumption and tissue saturation, SOD increases as does uncoupling, lipid peroxidation and high levels of malondialdehyde (MDA) are observed with excess lipid peroxidation (Chen & Li, 2016). SOD can be counteracted by glutathione (SOD/G ratio) but this diminishes over time. This enhances the reductive state and perpetuates the gain of electrons, which are a hallmark of damaged physiology and shift efficient energy production away from oxidative metabolism of glucose and metabolic inflexibility.

 

PUFA, like DHA does initiate mitochondrial uncoupling but it’s inefficient and increases SOD degrading aerobic metabolism, which comes at a cost to lifespan. Hulbert notes that a 24% decrease in PI, is associated with doubling of lifespan and that calorific restriction alters the acyl composition of the cell membrane. Why?  Because PUFA are removed from the cell membrane to be used as fuel. Again this can be problematic if you persistently use unsaturated fatty acids as fuel. Not to mention that refeeding fasted subjects and those on a ketogenic diet are well known to depress thyroid hormone responsiveness, thyroid hormone receptors and glucose tolerance(Boelen, Wiersinga, & Fliers, 2008)(Garbow et al., 2011)(Kose, Guzel, Demir, & Arslan, 2017). Yes there are indeed many short-term studies showing positive changes from CR and ketogenic dieting. If one can benefit from these modalities great but if not metabolically flexible, it isn’t always going to be as fruitful as you think. It’s often these interactions that muddy the water between carbohydrate restriction and beneficial results. Hint, it’s never usually the carbohydrate, and if you’ve been prone to over eating, then that calorie deficit is always going to show a temporary positive effect.

If you’re someone that has tried many different interventions for improved health or even body composition and failed to get the results that you need, then the body requires a level playing field of energy and nutrients to create balance. Further stress from skipping meals, long hours without eating and failure to meet metabolic demands are some of the reasons why many develop metabolic inflexibility. The more stressed your physiology, the more prone it is to activating stress pathways and suppressing thyroid hormone, decreasing insulin responses and creating inflammation. More often than not those with tis existing inflexibility may not benefit from increased fatty acid oxidation mediated by a lack of available glucose.

Thyroid, PUFA and membrane composition and fluidity

My understanding of the so-called membrane, membrane pump theory and even membrane fluidity is certainly not of an expert but If I’m wrong here, I’m certainly willing to throw my hands up on in the air and say – I told you I wasn’t an expert.  I am reasonably sure of the interactions of thyroid hormone, its generality, it’s actions, organizational qualities and much like the theories of low serotonin, low estrogen, high cholesterol treated by statins, and that glyphosphate is a safe and friendly compound, that people with vested interests promote otherwise. I’m not going to go into the complexities of Gilbert Ling’s work (Gilbert N. Ling, 1965 1997, 2014) I’d be lying if I said I truly understand it but my attempt to summarize such a vast body of work.

The membrane pump theory has been a widely accepted unproven theory that appears on paper, to be unable energetically to support and each pump requiring unaccountable levels of ATP. Ling’s work suggests that membrane interactions are largely supported by organised or structured water interfaces and that there is no cellular membrane to speak of. Thyroid hormone, proteins and cholesterol are other integral components of this interface.

It’s always contentious when someone ends up disproving a theory that’s widely accepted without being proven.

Does it make sense that during fasting, these essential PUFA’s are depleted from this so-called membrane and replaced with cholesterol? Can they really be that essential? Thyroid hormones have been shown to modify this “membrane permeability”, cooperatively influencing behavior of enzymes and can penetrate the phospholipid bilayers  (Issé, Yunes Quartino, Fidelio, & Farías, 2013). Triiodothyronine or T3 appears similar to cholesterol’s action, increasing fluidity in ordered gel phases and decreasing in liquid crystalline states of phospholipids. I’m guessing that alterations in structured water through positive/ negative charges, and interactions between organisational qualities of thyroid hormones and cholesterol could be the ideal interface. This may explain why in hypothyroidism the so-called membrane, becomes more disorganised, less gel like and more abundant in PUFA (PUFAs degrade cholesterol).

 Restriction of PUFA, methionine and other agents which reduce biology need to be compared with so called decreased rate of living theories to ascertain what really increases longevity. If we keep looking at theories that promote decreased function instead of maintaining and improving order. The end result may be decreased lifespan and a slow death of cellular function.

 

References:

Boelen, A., Wiersinga, W. M., & Fliers, E. (2008). Fasting-Induced Changes in the Hypothalamus–Pituitary–Thyroid Axis. Thyroid, 18, 12–129. https://doi.org/10.1089/thy.2007.0253

Chen, Y., & Li, P. (2016). Fatty acid metabolism and cancer development. Science Bulletin, 61(19), 1473–1479. https://doi.org/10.1007/S11434-016-1129-4

Garbow, J. R., Doherty, J. M., Schugar, R. C., Travers, S., Weber, M. L., Wentz, A. E., … Crawford, P. A. (2011). Hepatic steatosis, inflammation, and ER stress in mice maintained long term on a very low-carbohydrate ketogenic diet. American Journal of Physiology - Gastrointestinal and Liver Physiology. https://doi.org/10.1152/ajpgi.00539.2010

Hulbert, A. J. (2007). Membrane fatty acids as pacemakers of animal metabolism. In Lipids. https://doi.org/10.1007/s11745-007-3058-0

Hulbert, A. J., Kelly, M. A., & Abbott, S. K. (2014). Polyunsaturated fats, membrane lipids and animal longevity. Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology. https://doi.org/10.1007/s00360-013-0786-8

Issé, B. A., Yunes Quartino, P., Fidelio, G. D., & Farías, R. N. (2013). Thyroid hormones-membrane interaction: Reversible association of hormones with organized phospholipids with changes in fluidity and dipole potential. Chemistry and Physics of Lipids. https://doi.org/10.1016/j.chemphyslip.2013.08.007

Kose, E., Guzel, O., Demir, K., & Arslan, N. (2017). Changes of thyroid hormonal status in patients receiving ketogenic diet due to intractable epilepsy. Journal of Pediatric Endocrinology and Metabolism. https://doi.org/10.1515/jpem-2016-0281

Ling, Gilbert N. (1997). Debunking the Alleged Resurrection of the Sodium Pump Hypothesis. Physiological Chemistry and Physics and Medical NMR.

Ling, Gilbert N. (2014). Canwe see living structure in a cell? Physiological Chemistry and Physics and Medical NMR.

Ling, Gilbert Ning. (1965). THE PHYSICAL STATE OF WATER IN LIVING CELL AND MODEL SYSTEMS. Annals of the New York Academy of Sciences. https://doi.org/10.1111/j.1749-6632.1965.tb45406.x

Madison Sullivan, E., Pennington, E. R., Sparagna, G. C., Torres, M. J., Darrell Neufer, P., Harris, M., … Shaikh, S. R. (2018). Docosahexaenoic acid lowers cardiac mitochondrial enzyme activity by replacing linoleic acid in the phospholipidome. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.M117.812834

Speakman, J. R., Talbot, D. A., Selman, C., Snart, S., McLaren, J. S., Redman, P., … Brand, M. D. (2004). Uncoupled and surviving: Individual mice with high metabolism have greater mitochondrial uncoupling and live longer. Aging Cell. https://doi.org/10.1111/j.1474-9728.2004.00097.x

Vaanholt, L. M., Daan, S., Schubert, K. A., & Visser, G. H. (2009). Metabolism and Aging: Effects of Cold Exposure on Metabolic Rate, Body Composition, and Longevity in Mice. Physiological and Biochemical Zoology. https://doi.org/10.1086/589727

http://raypeat.com/articles/

http://www.gilbertling.org/

 

Body temperature and health

Most people are so confused as to what constitutes good health these days and when they turn up to my office in low metabolic states with digestion, sleep, energy, mood and other issues. One of the first things that they say is that they eat really healthily. If you throw into the melting pot the obsession with the keto diet, chronic calorific restriction (CR) or other modalities, those short term gains have turned into long term deficits. I’ve long opined that health in general terms can be defined by:

 

·      Good energy

·      Good Digestion 2-3 bowel movements per day

·      Restorative sleep

·      Balanced mood free of depression or anxiety

·      Desire for life, motivation, hobbies and interests

·      Healthy libido

·      Absence of pain

Humans are endotherms that regulate their temperature at 37 degrees centigrade.jpg

What does your body temperature suggest about your health?

Get cold…read on

I’ll also add to that list a warm body and the ability to generate efficient energy,  a phrase biologists might use is a state of negative entropy. Entropy is a state associated with decay and disorder and as entropy increases, equilibrium is achieved - where a state of no energy in and no energy out or death of a living system occurs. The basis for life and metabolism is governed by the enzymes. Enzymes function well in an appropriate temperature and in a medium that is neither too acidic nor too alkaline. Mammals and specifically humans are endotherms that regulate their temperature in  tight range at approximately 37 degrees Centigrade (C) or 98.6 Fahrenheit (Bicego, Barros, & Branco, 2007). The central compartment theory of temperature  suggests that the head and the core should maintain a relatively stable temperature, due to the rich vascular supply and that the periphery may vary some 2-4 C.  

In a recent study that I conducted I suggested that the peripheral and core temperatures should remain at a similar level of about 37 C . The suggestion that a decreased body temperature recorded in the head, might be the last place that you would see a reduction due to the large quantities of glucose that the brain uses to maintain function. It’s possible to suggest that the slowing of function in low energy and hypothyroid states might be observed initially in the trunk or core. The well documented symptoms of constipation, decreased heart rate, slowed contraction relaxation of the heart and arteries and reduced peripheral relaxation of tendons (Achilles tendon reflex) might appear in the trunk and peripherally due to the preferential oxidation of glucose initially. Due to the vast systemic implications of low thyroid function, many different paths of decreased function might occur, dependant on nutrition, environmental stimulus and other stressors. In my study I didn’t find this but what I did find is strong linear correlations between low body temperature in both the mouth and armpit, multiple low thyroid symptoms (mean 6.8 per subject) and yet normal blood values.

Humans are endotherms that regulate their temperature at 37 degrees centigrade-2.jpg

Thyroid hormone affects all aspects of biology

 

There are many factors that can decrease body temperature such as CR, fasting, estrogen, stress, pollution, over exercise and more. CR has been suggested as a mechanism for maintaining longevity but studies lack any conclusive evidence (Carrillo & Flouris, 2011) and a theory that a cold body, decreases metabolism, oxidation and damage therefore preserving tissues. Another emergent theory and results show in rodent studies, that mammals with a high energy intake, high metabolism and organised biology can increase life span (John R. Speakman et al., 2004) (J. R. Speakman, 2005). Think about this for a minute:

Calorific restriction makes the body cold, decreases metabolic rate  (via inhibition of thyroid hormone) and disorganisation of tissues. Entropy State

Adequate energy, maintains body temperature and organises tissues to function at their best. Negative entropy state.

From an evolutionary perspective fasting due to lack of food was a necessity. Fasting these days could be a useful tool, if you were prone to constant overeating but if your system lacks the flexibility to do so problems can occur. That’s not to say that calorie restriction for weight loss isn’t helpful but sustained CR in a system that doesn’t respond well might be counterproductive. Pollution has increased at a phenomenal rate clearly affecting physiology and hormones (Gore et al., 2015). Does it make sense that a so called detox diet, low in calories, protein, carbohydrates can enhance the function of detoxification, when liver function is energy and thyroid dependant? Skipping breakfast alone in some is associated with increased cortisol, glucagon and metabolic inflexibility (Jakubowicz, Wainstein, Ahren, et al., 2015) (Jakubowicz, Wainstein, Ahrén, et al., 2015). These factors can also decrease the mitochondrial uncoupling proteins which are responsible for increased body temperature.

Ageing is also associated with decreased metabolic rate, colder bodies and accepted increases in thyroid hormone stimulating values (TSH) (Laurberg, Andersen, Pedersen, & Carlé, 2005) . If symptoms of failing biology are present with isolated thyroid symptoms such as increased cholesterol,  , high blood pressure and sugar, cardiovascular issues and even cancer the acceptance of TSH and other thyroid hormone analysis to accurately predict hypothyroidism should be considered. Body temperature and metabolic rate was reliably used in the last century to diagnose hypothyroidism with qualitative analysis of symptoms and symptoms resolved with thyroid hormone treatment (Barnes, 1942) (McGavack, Lange, & Schwimmer, 1945) (Peat, 1999). Whilst thyroid is useful for restoring function, food and other factors can be used to restore and maintain function (previous blog on maintaining the aerobic system)

Certain nuances exist in temperature regulation that are dependant on acute or chronic exposure to stressors and a slowing down of the system through  a functionally, subclinical or overt hypothyroid state. In short term fasting, TSH is initially raised then decreases, negating thyroid blood tests. In the same manner the time frame of any stressor can dictate whether short or long term compensations of  the sympathetic adrenergic system is supporting the system. In well established feedback mechanism it’s known that as TSH increases so does cortisol and as body temperature approaches hypothermic levels (around 35C) cortisol, adrenaline and noradrenaline can increase body temperature as a protective response.

In a world where excess environmental and social stressors are ever increasing - it might make sense to maintain an efficient, organised warm body rather than reducing its function and heat.

 

References:

 

Barnes, B. (1942). Basal temperature versus basal metabolism. Journal of the American Medical Association, 119(14), 1072–1074. http://doi.org/10.1001/jama.1942.02830310006003

Bicego, K. C., Barros, R. C. H., & Branco, L. G. S. (2007). Physiology of temperature regulation: Comparative aspects. Comparative Biochemistry and Physiology - A Molecular and Integrative Physiology. http://doi.org/10.1016/j.cbpa.2006.06.032

Carrillo, A. E., & Flouris, A. D. (2011). Caloric restriction and longevity: Effects of reduced body temperature. Ageing Research Reviews. http://doi.org/10.1016/j.arr.2010.10.001

Gore, A. C., Chappell, V. A., Fenton, S. E., Flaws, J. A., Nadal, A., Prins, G. S., … Zoeller, R. T. (2015). Executive Summary to EDC-2: The Endocrine Society’s second Scientific Statement on endocrine-disrupting chemicals. Endocrine Reviews. http://doi.org/10.1210/er.2015-1093

Jakubowicz, D., Wainstein, J., Ahrén, B., Bar-Dayan, Y., Landau, Z., Rabinovitz, H. R., & Froy, O. (2015). High-energy breakfast with low-energy dinner decreases overall daily hyperglycaemia in type 2 diabetic patients: a randomised clinical trial. Diabetologia, 58(5), 912–919. http://doi.org/10.1007/s00125-015-3524-9

Jakubowicz, D., Wainstein, J., Ahren, B., Landau, Z., Bar-Dayan, Y., & Froy, O. (2015). Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 Diabetes: A randomized clinical trial. Diabetes Care, 38(10), 1820–1826. http://doi.org/10.2337/dc15-0761

Laurberg, P., Andersen, S., Pedersen, I. B., & Carlé, A. (2005). Hypothyroidism in the elderly: Pathophysiology, diagnosis and treatment. Drugs and Aging. http://doi.org/10.2165/00002512-200522010-00002

McGavack, T. H., Lange, K., & Schwimmer, D. (1945). Management of the myxedematous patient with symptoms of cardiovascular disease. American Heart Journal. http://doi.org/10.1016/0002-8703(45)90476-5

Peat, R. (1999). Thyroid Therapies, Confusion and Fraud. Retrieved from www.raypeat.com/articles/articles/thyroid.shtml

Speakman, J. R. (2005). Body size, energy metabolism and lifespan. Journal of Experimental Biology. http://doi.org/10.1242/jeb.01556

Speakman, J. R., Talbot, D. A., Selman, C., Snart, S., McLaren, J. S., Redman, P., … Brand, M. D. (2004). Uncoupled and surviving: Individual mice with high metabolism have greater mitochondrial uncoupling and live longer. Aging Cell. http://doi.org/10.1111/j.1474-9728.2004.00097.x

 

Is your functional training making you dysfunctional?

Buzz words of the last decade in the health and fitness industry were terms such as functional, core, ground reaction, Paleo, intermittent fasting etc etc. It is an easy approach for people to throw around these types of phrases, impressing clients without having a true understanding of what they really mean. Like many it took me some time to realise that to get people strong you need a combination of good therapy, improved movement patterns and ultimately lifting well.  The emphasis on functional training has contributed to increased facilitation patterns which contribute to musculo-skeletal issues, much in the same way that the circuit training phase of the 90’s did. Now there are increased loads and patterns of dysfunction by methodologies such as Boot Camps, Cross Fit, TRX classes, Endurance events and the like and more than ever, I (and my peers) am seeing the incidence of overuse injuries created by inhibition and facilitation from poorly constructed exercise programming.

Let’s take this guy below. His exercise using the TRX must be functional , it must be making him strong right? Well no and here’s why? This gym dude like millions of others makes the mistake of utilising balance with strength as an exercise. The net effect of this type of exercise is facilitation when there is instability without the ability to stabilise.

trxjpg

You can clearly note here a rounding of the upper back   and cranial extension caused by inability to stabilise using the cervical flexors, mid and lower trapezius.

Facilitated                                                                          Inhibited

Upper traps/Scalenes                                                     Cervical flexors

Levator Scapula                                                              Middle and lower trapezius

Pec minor and probably major in this case                    Latissimus dorsi

Sternocleidomastoid                                                      Subscapularis and other structures

The cervical extensors, upper traps and pec minor amongst other structures have the ability to disrupt breathing patterns, gait and decrease strength in patterns such as the squat and dead lift. Those who teach these type of exercises should be skilled in spotting movement dysfunction, inhibition and facilitation and understand strategies of how to correct these issues or at least understand that if you keep exercising in this way you will lead to breakdown of key stabilising structures.

Is it a ‘core’ problem?

The core is really the interaction of all the muscles in the body but specific attention has been paid areas such as the ‘inner unit’ which comprises of the Tranversus Abdominus (TrA), multifidus, diaphragm and pelvic floor and the outer unit which comprises of the abdominals and internal and external obliques which interlink with many larger muscles.  In reality these muscles work in tandem with other muscles to create structural balance.  Many people think that to train their core they have to blitz their abdominals, obliques and back muscles with intensity which creates dysfunction.

This is where common misconceptions occur. The core more often than not, needs to be recruited appropriately and that should occur with proper movement development and determining what other structures beyond the core (such as previous injuries) are prevalent. Many of these problems can occur as a result of many factors. Children who don’t develop crawling patterns, who are either rushed into walking or put into baby crawlers can be at risk in later life of poor breathing patterns and core dysfunction. The seated position is not great for the spine and muscles can develop inhibition as other muscles get overworked and the nervous system will always take the least path of resistance when it comes to movement and muscle activation. Additionally the seated position also helps to create inverted breathing patterns, which disrupts the stabilising capacity of core muscles.

Many people make the mistake of activating the TrA in all the time (or drawing the belly in), even when walking. This is a disaster as it creates facilitation of the accessory muscles of breathing, creating a forward head posture, rounded back and weak links in the chain from head to the toe. In fact in some schools of thought letting your belly out and pushing outwards  also increases abdominal pressure and stabilising mechanisms that are just as good if not better for ‘core’ recruitment. Sometimes we are so fixated about our weight that we constantly walk around with our belly drawn in…let it hang out I say.

References:

  1. DNS technique according to Kolar. Training Manual Rehabilitation School of Prague
  2. Hodges, P. W. Is there a role for Transversus Abdominis in Lumbo-Pelvic  Stability? Manual Therapy (1999) 4(2), 74±86
  3. Kolá, P. Importance of Developmental Kinesiology for Manual Medicine.1996
  4. Weinstock, D. Neuro Kinetic Therapy. North Atlantic Books 2010