What Hibernating Bears Might Teach us About Chronic Illness

A question I’ve held for over 20 years is whether biological states that cause disease, and which are seen as abnormal – such as lack of insulin and high blood sugar levels in type 1 diabetes; high blood sugar levels, elevated insulin and insulin resistance in type 2 diabetes, and exhaustion in chronic fatigue syndrome (ME/CFS) – exist elsewhere in normal states of health or as appropriate adaptations to circumstances.

My training as a somatic trauma therapist supported a sense that symptoms are intelligent. What was proposed in my new field of study after leaving medicine was that symptoms can reflect an impulse that has been thwarted, overridden or frozen in time, such as from overwhelming experiences and trauma.

As a trauma therapist, my personal work with clients as well as with my own disabling symptoms of chronic fatigue has further supported this view that facilitating previously thwarted impulses to manifest and express themselves in gently supported ways can help symptoms to resolve. The understanding is that these actions, big and small, visible and invisible, external and internal, convey a message to the nervous system that stops the danger signaling and threat physiology that has been driving symptoms, such as pain in a specific area of the body that was once physically harmed or unable to defend you as intended in a threatening situation.

Over the years I’ve discovered intriguing research that further supports these perspectives, including about threat physiology, with respect to chronic illness. It also supports observations by somatic trauma therapists and other health professionals and people working with their health from trauma perspectives around the world.

The first finding is from a small study of people with chronic fatigue. The second is about the physiological state of bears in hibernation, which I’ve been so looking forward to sharing with you. Both suggest that the drivers of chronic illness come from bodies whose physiologies are caught in a prolonged threat response or what we might call a “cell danger response,” “threat physiology” or “survival physiology.”

Chronic Fatigue: a Metabolic State of “Dauer”

In 2016 Professor of Medicine, Pediatrics, and Pathology at the University of California, San Diego (UCSD) Robert Naviaux, MD, PhD, who is also a virologist, and molecular and cell biologist, published the results of a small study of people with myalgic encephalitis / chronic fatigue syndrome (ME/CFS or CFS).

Naviaux and his team had collected blood samples from 45 people with ME/CFS meeting multiple well-accepted diagnostic criteria and 39 healthy controls matched for age and gender.

They analyzed 612 metabolites from 63 biochemical pathways.

20 of these metabolic pathways had abnormalities. 

What struck them was that 80% percent of these abnormalities involved metabolites that reflected decreases in activity. They noted these were consistent with a state of low metabolic function that reflects a process linked to shutting down.

These labs were chemically similar to what is found in the natural response of c. elegans, a worm used in many kinds of research studies, when it enters “dauer.” Dauer is a state of arrested development that occurs when c. elegans encounters circumstances in its environment that are not conducive to survival – such as when food, water, oxygen levels or temperatures are too low. The state of dauer enables c. elegans to reduce metabolism in order to optimize its ability to wait until circumstances improve. Then its system shifts and it continues its development.

Despite all the different histories, onset triggers and experiences of people in the study with ME/CFS, their chemical signatures were similar. Different “causes” yet similar effects and symptoms.

The Naviaux team’s conclusion was that ME/CFS reflects a body caught in a cell danger response (CDR), which, after being unable to overcome one or more threats, has become prolonged.

The cell danger response (CDR) is the evolutionarily conserved metabolic response that protects cells and hosts from harm. It is triggered by encounters with chemical, physical, or biological threats that exceed the cellular capacity for homeostasis ⁽¹⁾Naviaux, R. K. (2013, Aug 24). Metabolic features of the cell danger response. Abstract. Mitochondrion. https://doi.org/10.1016/j.mito.2013.08.006 . 

Their assessment is similar to somatic trauma therapy perspectives in which symptoms such as PTSD, anxiety, depression, and chronic pain reflect a body caught in prolonged threat physiology ⁽²⁾Levine, P. (1997). Waking the tiger: Healing trauma. North Atlantic Books. https://www.amazon.com/Waking-Tiger-Healing-Peter-Levine/dp/155643233X, ⁽³⁾Scaer, R. (2005). The trauma spectrum: Hidden wounds and human resiliency. W.W. Norton. https://www.amazon.com/Trauma-Spectrum-Hidden-Wounds-Resiliency/dp/0393704661/ref=sr_1_2?ie=UTF8&qid=1536248014&sr=8-2&keywords=ROBERT+SCAER, ⁽⁴⁾Yehuda, R., & Seckl, J. (2011, Dec). Minireview: Stress-related psychiatric disorders with low cortisol levels: A metabolic hypothesis [Review]. Endocrinology, 152(12), 4496-4503. https://doi.org/10.1210/en.2011-1218 . These symptoms are the result of traumatic experiences the system was too overwhelmed to successfully navigate and overcome. Naviaux also applies cell danger response theory to chronic illness.

When the CDR persists abnormally, whole body metabolism and the gut microbiome are disturbed, the collective performance of multiple organ systems is impaired, behavior is changed, and chronic disease results ⁽⁵⁾Naviaux, R. K., Naviaux, J. C., Li, K., Bright, A. T., Alaynick, W. A., Wang, L., Baxter, A., Nathan, N., Anderson, W., & Gordon, E. (2016, Aug 29). Metabolic features of chronic fatigue syndrome. Proceedings of the National Academy of Sciences of the United States of America, 113(37), E5472-5480. https://doi.org/10.1073/pnas.1607571113 
p. E5472–E5480.

It felt extraordinarily supportive to find that an entirely different field of study had come to similar conclusions identified in the field of trauma therapy. Even more powerful was that cell danger response theory identified objective, measurable findings with chemicals in the blood that were consistent with a state of shut down.

In the field of traumatic stress trauma occurs following an experience that is so overwhelming that it elicits this shut down response. Shutting down is directed by the nervous system and is not a conscious choice. It may take the form of pure physiological collapse sometimes referred to as “Faint.” It may also occur after an overriding signal tells a system already in a sympathetic state of fight or flight, fear or intense activation to shut down into a death-like state, in which case it is referred to as “freeze.” Freeze states include biology that is both “wired” in sympathetic and “tired” in parasympathetic whereas “faint and collapse” reflect states that are more purely shut down mediated. Both are regulated by the dorsal vagus, which is the slow, primal, unmyelinated branch of the vagus described in polyvagal theory ⁽⁶⁾Porges, S. W. (2004). Neuroception: A subconscious system for detecting threats and safety. Zero to Three, May, 19-24. https://www.semanticscholar.org/paper/NEUROCEPTION%3A-A-Subconscious-System-for-Detecting-Porges/7aa83dc8d507fc38aa97e22233d96fd878ff7e51. To keep things simple I often use just the term freeze to represent the continuum of states of shut down even though this is not always technically accurate.

Freeze, faint, collapse and shut down occur in our physiology during situations too threatening to overcome. They happen when other, first-line protective mechanisms aren’t available, possible or successful. This includes times when the most energy-efficient form of self-protection of social engagement, which might include talking, setting a boundary or using the power of the group for solidarity or protection (social nervous system / smart vagus) is not an option. It occurs when more physically demanding defense mechanisms such as action and fight or flight (sympathetic nervous system) fail or aren’t options either.

The state of dauer in c. elegans compares in at least some ways to a traumatic experience of freeze or faint in that it is activated when other options for survival are not going to be able to overcome a particular circumstance.

Cell danger theory proposes that the cause of chronic illness is prolonged cell danger signaling. It suggests that treatment for chronic illnesses of all kinds is therefore to turn off these signals of threat. Naviaux and his team are exploring medications that may serve this purpose ⁽⁷⁾Naviaux, R. K., Curtis, B., Li, K., Naviaux, J. C., Bright, A. T., Reiner, G. E., Westerfield, M., Goh, S., Alaynick, W. A., Wang, L., Capparelli, E. V., Adams, C., Sun, J., Jain, S., He, F., Arellano, D. A., Mash, L. E., Chukoskie, L., Lincoln, A., & Townsend, J. (2017, Jul). Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial. Ann Clin Transl Neurol, 4(7), 491-505. https://doi.org/10.1002/acn3.424. My own curiosity has been whether healing trauma, such as through trauma therapy, can be effective given that it is already available and does not require waiting for others to come up with new treatment solutions that do not yet exist.

This leads me to my fascination with discoveries made in hibernating bears.

Hibernating Bears

During hibernation, a bear’s physiology enters a state that appears, at least in general terms, to be quite similar to dauer in c. elegans and other states of shut-down designed to out wait a threatening situation. Hibernation is a brilliant natural survival strategy that enables a mammal to overcome an otherwise inescapable, life-threatening situation: Winter.

Because hibernation reflects a state of such significant decreases in metabolism such as lowered heart rate, blood pressure, and movement, I long wondered what a bear’s winter physiology looked like. Might it have similarities to anything we see in chronic illness? Might it be similar to freeze and other shut-down states that can result from trauma?

I would regularly search online to see if more had been learned about hibernation. In 2014 those studies finally started showing up. My nerdy, curious self who lives in what I consider to be a state of relative freeze of wired and tired ME/CFS has been deeply fascinated by what they found.

Fat Grizzlies Do Not Develop Type 2 Diabetes

A group of researchers in the state of Washington in the USA looked at the state of hibernation in their group of captive outdoor Grizzly bears.

Their initial question was whether the process of gaining a lot of weight in preparation for hibernation made the bears insulin resistant.

Insulin is the energy storage hormone. It helps the body store sugar, including as fat, to keep reserves available so that the body doesn’t run out, such as in between meals or during times of high energy usage, such as in exercise. Insulin resistance is a state in which the body and its cells are less able to utilize insulin and can then end up being unable to absorb sugar, thus leaving more sugar in the blood than is seen in good health.

The researchers’ question came from the current perspective in medicine that obesity is the cause of insulin resistance, and that it is the fact of being overweight that causes increases in blood sugar levels in prediabetes, type 2 diabetes and a number of other chronic illnesses.

The Washington researchers tested their theory when the bears were at their highest weight just before hibernation. They assumed the bears would be highly insulin resistant. They

Injected them with what they thought was a tiny dose of insulin, about the same amount you would give to a human.

The bears almost died of insulin overdose ⁽⁸⁾Manke, K. (2014, August 5). Why Fat Grizzlies Don’t Get Diabetes Like We Do [Treatments]. NPR. https://www.npr.org/sections/health-shots/2014/08/05/338045480/why-fat-grizzlies-dont-get-diabetes-like-we-do.

The researchers were astounded. The degree to which the bears were not only NOT insulin resistant but instead highly SENSITIVE to insulin seemed contradictory to the main theory we have that high weight in humans is the cause of insulin resistance. They decided to explore further.

They learned that when bears enter the fall season of preparation for hibernation their insulin sensitivity actually RISES significantly, helping their bodies more easily and quickly store the fat they’ll need for surviving the winter.

Then, with hibernation, the bears’ physiology shifts and they became Insulin Resistant.

Insulin Resistance

Insulin is a hormone produced in the pancreas that helps the body regulate sugar levels and keep levels within a certain range. Insulin assists the body to absorb sugar into the cells of the liver, muscle and fat so it can be used later.

Our understanding of the function of insulin in humans is that tissues become “resistant” to insulin in the fight/flight response. This is a natural adjustment in the moment that prevents absorption of sugar into cells in order to make sugar more available in the blood. The availability of sugar allows it to be used as energy by the brain, muscles and other organs during such states of heightened need and demand.

In health, our bodies shift the degree of insulin sensitivity and resistance throughout the day to adjust to circumstances.

Insulin Resistance in Hibernating Bears

During hibernation in bears, metabolism shifts from using sugar as the primary source of fuel in the spring, fall and summer when food is available, to the use of stored fat as fuel when food is unavailable in winter. The process of metabolizing fat also releases water, providing hydration since bears do not eat or drink during hibernation. States of Insulin Resistance facilitate the utilization of fat as fuel.

When spring arrives, temperatures begin to warm, and food becomes available the bears emerge from hibernation and their physiologies shift again, back to a state of insulin sensitivity.

“I look at it as a dimmer switch within the tissue,” says Corbit, referring to how the cells turn their sensitivity to insulin up and down ⁽⁹⁾Manke, K. (2014, August 5). Why Fat Grizzlies Don’t Get Diabetes Like We Do [Treatments]. NPR. https://www.npr.org/sections/health-shots/2014/08/05/338045480/why-fat-grizzlies-dont-get-diabetes-like-we-do .

Hibernation: A State of Adaptation

The regulation and activity of insulin is influenced by the environment and is not a fixed state. The degree of insulin sensitivity and resistance is something that, in health, is adaptive to specific situations.

Other studies have also identified bears in hibernation as being in states of insulin resistance, including in black bears and brown bears and bears in Europe as well as the USA. Findings vary a little depending on the weather and availability of food such as warmer winters and availability of sources of fuel such as nuts ⁽¹⁰⁾North American Bear Center. 5 Stages of Activity and Hibernation: The annual cycle of black bear activity and hibernation has five stages https://bear.org/5-stages-of-activity-and-hibernation/. Some studies have found that hibernating bears have

• higher levels of cholesterol, triglyceride and LDL levels ⁽¹¹⁾Arinell, K., Sahdo, B., Evans, A. L., Arnemo, J. M., Baandrup, U., & Fröbert, O. (2012, Jun). Brown bears (Ursus arctos) seem resistant to atherosclerosis despite highly elevated plasma lipids during hibernation and active state. Clinical and Translational Science, 5(3), 269-272. https://doi.org/10.1111/j.1752-8062.2011.00370.x ,
• decreased kidney function during this time when they do not urinate
• suppression of bone remodeling, which conserves energy and bone mass ⁽¹²⁾McGee-Lawrence, M., Buckendahl, P., Carpenter, C., Henriksen, K., Vaughan, M., & Donahue, S. (2015). Suppressed bone remodeling in black bears conserves energy and bone mass during hibernation. Journal of Experimental Biology, 218(13), 2067-2074. https://doi.org/10.1242/jeb.120725 .
• a hypothyroid state (low thyroid), an adaptation that decreases metabolism ⁽¹³⁾McCain, S., Ramsay, E., & Kirk, C. (2013, 06/01). The effects of hibernation and captivity on glucose metabolism and thyroid hormones in American black bear (Ursus Americanus). Journal of Zoo and Wildlife Medicine, 44, 324-332. https://doi.org/10.1638/2012-0146R1.1 .

In humans, lifestyle factors such as a high fat diet when combined with high carbs, and low levels of exercise and activity are considered important causes of obesity and also of chronic illness, including diseases associated with Insulin Resistance such as type 2 diabetes, heart disease and bone loss (osteoporosis).

After months of minimal activity and a high fat diet during hibernation, bears show no evidence of heart disease, no indications of high blood sugar levels or diabetes, and no signs of osteoporosis ⁽¹⁴⁾Jansen, H. T., Trojahn, S., Saxton, M. W., Quackenbush, C. R., Evans Hutzenbiler, B. D., Nelson, O. L., Cornejo, O. E., Robbins, C. T., & Kelley, J. L. (2019). Hibernation induces widespread transcriptional remodeling in metabolic tissues of the grizzly bear [Abstract]. Commun Biol, 2, 336. https://doi.org/10.1038/s42003-019-0574-4.

Inactivity, increased weight and a fat based diet in bears, in other words, is not a cause of disease.

The question researchers are asking is why don’t bears develop type 2 diabetes (or, for that matter, the other diseases associated with insulin resistance)? They suspect the chemical pathway will provide information to help in preventing and treating diabetes ⁽¹⁵⁾Skett, P. (2014, Aug). Grizzly bears become ‘diabetic’ when they hibernate. New Scientist. https://www.newscientist.com/article/dn26008-grizzly-bears-become-diabetic-when-they-hibernate/ .

The Goal: Stop Cell Danger Signaling

The premise of trauma science is that adversity and experiences overwhelming or threatening enough to elicit a shut down or freeze response can interrupt the ability of our physiology to shift. Over time, if we have enough exposures to adversity to strengthen such an altered cell danger response pathway, our bodies begin to solidify towards states of prolonged threat physiology.

The perspective in the world of somatic trauma therapy is that this happens because experiences of freeze do not give the brain the message that we have survived. Our brains thus perceive we are still under threat. They adapt to this perception with threat physiology to protect us, such as staying in freeze to out wait the danger.

Helping the body access the impulses to “unfreeze,” thaw, and escape through trauma therapy is one way in which we can stop that signaling of danger and enable the body to return to its natural ability to shift gears ⁽¹⁶⁾Yehuda, R., Daskalakis, N. P., Desarnaud, F., Makotkine, I., Lehrner, A. L., Koch, E., Flory, J. D., Buxbaum, J. D., Meaney, M. J., & Bierer, L. M. (2013). Epigenetic biomarkers as predictors and correlates of symptom improvement following psychotherapy in combat veterans with PTSD. Front Psychiatry, 4(Article 118), 1-14. https://doi.org/10.3389/fpsyt.2013.00118, ⁽¹⁷⁾Yehuda, R., Spiegel, D., Southwick, S., Davis, L. L., Neylan, T. C., & Krystal, J. H. (2016). What I have changed my mind about and why. European Journal of Psychotraumatology, 7, 1-7. https://doi.org/10.3402/ejpt.v7.33768.

Hibernation, Insulin Resistance and Freeze

I have been deeply fascinated by these findings of Insulin Resistance in the healthy, adaptive state of hibernation. It raises many questions for me as well.

Does hibernation have any relation to states such as dauer in c. elegans and low metabolic function in Chronic Fatigue?

Does our understanding of shut down states resulting from overwhelming situations that are experienced as traumatic have any relationship to the shut down physiology of hibernation? Both states can involve low blood pressure, reductions in heart rate, and behavioral as well as physiological expressions of being slowed or going into a death-like physiology. These shifts are not conscious and are regulated by the nervous system.

Bears naturally shift between states of insulin sensitivity and resistance. This is likely similar in humans given how, in health, our bodies naturally shift between digesting food, resting in between meals, and exercising, which all call for different utilizations of sugar and fuel throughout the 24 hour day.

This raises more questions.

Are chronic illnesses that are associated with states of Insulin Resistance, such as Type 2 Diabetes, reflective of physiologies

• caught in a survival strategy?
• stuck in shut down?
• expressing unresolved trauma?

One of the reasons I am so captivated by hibernating bears is that if Insulin Resistance is a response to trauma in humans, then understanding, addressing and healing trauma might revolutionize how we approach prevention and treatment.

Insulin Resistance as Biomarker and Opportunity

Insulin Resistance precedes the onset of Type 2 Diabetes by 10 to 15 years ⁽¹⁸⁾Ghani, Z. A., Qaddori, H., & Al-Mayah, Q. (2023, May). Triglyceride/high-density lipoprotein ratio as a predictor for insulin resistance in a sample of healthy Iraqi adults. Journal of Medicine and Life, 16(5), 668-674. https://doi.org/10.25122/jml-2022-0239, p. 672. This is a reminder that chronic illness does not emerge suddenly, “out of the blue,” and instead is the result of processes that develop over a long time like an undersea volcano ⁽¹⁹⁾Poser, C. M. (1986). Pathogenesis of multiple sclerosis. A critical reappraisal. Acta Neuropathol (Berl), 71(1-2), 1-10. https://doi.org/10.1007/BF00687954. We see this in autoimmune diseases, in which antibodies begin to arise 10 or more years prior to onset ⁽²⁰⁾see my blog post Trauma and Autoimmune Disease https://chronicillnesstraumastudies.com/trauma-autoimmune-disease/, ⁽²¹⁾Ziegler AG, Rewers M, Simell O, et al. Seroconversion to multiple islet autoantibodies and risk of progression to diabetes in children. JAMA 2013;309(23):2473-9, ⁽²²⁾Johnston C, Milward BA, Hoskins P, et al. Islet-cell antibodies as predictors of the later development of type 1 (insulin-dependent) diabetes. A study in identical twins. Diabetologia 1989;32:382-86, ⁽²³⁾
Arbuckle MR, James JA, Kohlhase KF, et al. Development of anti-dsDNA autoantibodies prior to clinical diagnosis of systemic lupus erythematosus. Scand J Immunol 2001;54(1-2):211-9, ⁽²⁴⁾Edwards CJ, Cooper C. Early environmental factors and rheumatoid arthritis. Clin Exp Immunol 2006;143(1):1-5. doi: 10.1111/j.1365-2249.2005.02940.x and can also resolve, regress and disappear such that an autoimmune illness like type 1 diabetes does not actually develop ⁽²⁵⁾Regnell, S. E., & Lernmark, A. (2017, Aug). Early prediction of autoimmune (type 1) diabetes. Diabetologia, 60(8), 1370-1381. https://doi.org/10.1007/s00125-017-4308-1.

I’ve heard some of you state directly how helpful it might have been to know you might be at risk and to have received a heads up 5 or 10 or 15 years before onset.

What this suggests is that, for anyone looking for early indicators of risk that might help them work to reduce their risk, Insulin Resistance serves as an indicator or what might be called a “biomarker.”

Do you have Insulin Resistance (Triglycerides/HDL)?

You can calculate whether you have Insulin Resistance using the quick formula on this page that uses numbers from your fasting cholesterol panel that divides triglycerides by HDL as a good proxy ⁽²⁶⁾Ghani, Z. A., Qaddori, H., & Al-Mayah, Q. (2023, May). Triglyceride/high-density lipoprotein ratio as a predictor for insulin resistance in a sample of healthy Iraqi adults. Journal of Medicine and Life, 16(5), 668-674. jQuery('#footnote_plugin_tooltip_31350_1_26').tooltip({ tip: '#footnote_plugin_tooltip_text_31350_1_26', tipClass: 'footnote_tooltip', effect: 'fade', predelay: 0, fadeInSpeed: 200, delay: 400, fadeOutSpeed: 200, position: 'center right', relative: true, offset: [17, 10], });,">https://doi.org/10.25122/jml-2022-0239)), ⁽²⁷⁾Oliveri, A., Rebernick, R. J., Kuppa, A., Pant, A., Chen, Y., Du, X., Cushing, K. C., Bell, H. N., Raut, C., Prabhu, P., Chen, V. L., Halligan, B. D., & Speliotes, E. K. (2024, 2024/02/01). Comprehensive genetic study of the insulin resistance marker TG:HDL-C in the UK Biobank. Nature Genetics, 56(2), 212-221. jQuery('#footnote_plugin_tooltip_31350_1_27').tooltip({ tip: '#footnote_plugin_tooltip_text_31350_1_27', tipClass: 'footnote_tooltip', effect: 'fade', predelay: 0, fadeInSpeed: 200, delay: 400, fadeOutSpeed: 200, position: 'center right', relative: true, offset: [17, 10], });:">https://doi.org/10.1038/s41588-023-01625-2)), ⁽²⁸⁾I first learned of this proxy in a video by Dr. Robert Lustig https://www.youtube.com/watch?v=C3rsNCFNAw8. I do not know anything else about the website other than this being the easiest calculator to use that I found and their guide on how to interpret your result seems reasonable. There does not appear to be a clear and accepted norm for what is considered “great,” “good,” and “high risk” so I am not attempting to provide guidelines here. There are also direct lab tests to measure insulin resistance. Ask your health professional for assistance in identifying whether you have Insulin Resistance if this is something new you are wondering about.

My goal is to not induce fear. My intention is to

1) propose an example of a biomarker that may help assess if you have some risk for symptoms or a potential source of symptoms that you may already have, and

2) provide an opportunity to consider whether addressing trauma may be helpful in healing and prevention for you.

Examples from Our Histories

From a conversation I had with one of you who read my blog and has Type 2 diabetes, I’ve learned that healing trauma while also working with diet has been successful for her in regulating blood sugar levels while also decreasing medications that help lower glucose (are you there Wren?). In addition, healing trauma has been helpful even in the face of the common history people typically have with type 2 diabetes, in that it tends to run in the family and across multiple generations. This is a potent example that healing trauma can make a difference and introduces the possibility that it may be helpful for many people with symptoms related to Insulin Resistance (IR), especially if other approaches such as the common prescription to lose weight and exercise, are either not helping, difficult to accomplish, or insufficient.

My own lab tests do not show Insulin Resistance using this calculation even though IR is twice as common in people with chronic fatigue (ME/CFS) compared with the general population ⁽²⁹⁾Maloney, E. M., Boneva, R. S., Lin, J. M., & Reeves, W. C. (2010, Sep). Chronic fatigue syndrome is associated with metabolic syndrome: results from a case-control study in Georgia. Metabolism: Clinical and Experimental, 59(9), 1351-1357. https://doi.org/10.1016/j.metabol.2009.12.019. Might Insulin Resistance reflect a body only in a more shut down state? Or, more likely, there are many pathways that facilitate faint and freeze and we don’t need all of them to have become prolonged in order to have a chronic illness.

I have had very low triglycerides (under 100) and high levels of the good cholesterol HDL (varying from 60s to 120) since before the onset of ME/CFS. Higher HDL is more commonly seen in women. It’s possible that my fairly low carb diet, which I’ve learned towards for a few decades because it makes me feel better, is part of the reason for this. More likely, I simply do not have IR as a component of my threat physiology affecting my fatigue.

This is an example of the nuance and complexity of trauma, threat physiology, and health. I have other indicators of shut down, however, such as

• low blood pressure
• frequent brain fog (an indication of dissociation and freeze that can also happen in fight/flight)
• constipation
• the inability to exercise with much intensity.
• My simple thyroid function tests (TSH) have been at the high end of normal for 15 years during the height of my ME/CFS, suggestive of my being low thyroid. Interestingly, my TSH has shifted markedly in the other direction in the past year towards a very solidly normal value. I suspect this is an indication of one aspect of my physiology shifting out of freeze as I keep addressing and healing old trauma patterns that serve as ongoing triggers and brief triggers that stimulate flares.

My flares of fatigue are rarely severe anymore, are shorter in duration, easier to recognize in relation to triggers, and typically resolve much more quickly than in the early days, sometimes within an hour or two of identifying the trigger and working through it.

The states underlying our symptoms have a lot of variation and for many of us, there are likely multiple pathways caught in survival mode that drive our symptoms and thus take time to address.

Has healing trauma made a difference for anyone else who may have or have had a state of Insulin Resistance?

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Type 2 diabetes and trauma: an example of risk factors for Insulin Resistance

Chronic fatigue and the Cell Danger Response (detailed post)

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