Are You Running On Empty?

What if I said to you that anxiety and depression are metabolic issues, that one way or another they relate to fuel, and that even though fueling metabolism isn’t the only thing, it’s an important thing, and it cannot be any other way.

What Am I saying here? Am I saying you can simply consume more sugar (fuel) and all your problems will miraculously go away? No I’m not, even though it is the truth to a certain degree. We need sugar for fuel, we need fuel for energy, and we need energy for protection against stress.

How stress is able to be met determines whether the stress will be damaging or beneficial. Stress can be increased by many things, and whether metabolic function can meet stress, varies significantly from person to person, as well as from one day to the next, depending on many factors, fuel being a very important one.

So, Am I saying lack of fuel is the cause of anxiety and depression, and that improving thyroid metabolism is the solution? No, not exactly. But it’s a big factor that is often overlooked, and is also often easy to adjust.

Mental dysregulation is directly related to stress. When stress exceeds or interferes with energy supply, a whole lot of metabolically problematic things can start to happen. Whether this leads to anxiety or depression issues, depends on a variety of factors, including brain and nervous system condition.

Fuel issues commonly arise due to insufficient intake or availability of fuel. They can also be the result of interference with the ability to properly use fuel, or because of the consumption of inappropriate or sub-optimal foods for fuel. This is tied in with the multitude of things which can either assist or inhibit fuel usage, including vitamin and mineral deficiencies, as well as how the brain functions. It isn’t black and white, but it can help to break it down, in order to understand it better.

In reality – no matter which angle you choose to look at it from – the degree and kind of stress a person is (and has been) exposed to is always important, but the way in which that stress is able to be met, metabolically speaking, can change things dramatically, even when circumstances haven’t improved.

To put it another way, many things are stressful, and how overall biological systems (including nervous system and brain function) use or handle stress, is closely related to metabolism and thyroid energy production. In some cases, a small stress can have a harmful impact, in other cases a big stress can be easily dealt with, or can even be beneficial.

I’m not at all saying the type of experiences a person has aren’t relevant. That’s not the purpose of this article. Life experiences are most relevant. But there is a difference between the impact of emotionally stressful or traumatic situations on the nervous system and brain, when metabolism is fueled and working well, compared to when it isn’t.

How stressful something is for you, has a powerful effect. You can often immediately notice what it does to digestion, sleep, anxiety, mood, skin, and other things. You can observe how the way you are affected by a particular situation, changes the way your body responds. Biology influences psychology and vice versa. But the impact of a specific kind of situation can vary greatly.

The way life experiences interact with the brain and nervous system, influences metabolic function, but the same is true in reverse. Talking about how supporting metabolism, can assist with how the whole system deals with difficult situations, does not take anything away from the importance of other parts of the system, like brain function, for instance.

All systems relate to thyroid energy production one way or another. When you interfere with thyroid metabolism, it has an overall effect. How it changes the way you interpret and feel about the outside world, is influenced by many physiological circumstances. When metabolic function is suppressed, this can more easily lead to a downward spiraling vicious circle, that can prevent the whole from functioning well.

So can it be fixed, and how to fix it? If you’re after a simple, ‘it’s your genes’ kind of solution, I’m afraid I don’t have that for you. And I don’t believe that ever turns out to be a solution anyway. More likely just a diversion.

It’s true that hereditary factors can make a person more or less sensitive to the impact of stress, but the common argument that things like depression come down to genetics, seems to me to be misleading and unhelpful. Unless when you say ‘genetics’, what you mean is biology. In which case yes, many biological factors have a role to play

Mostly however, when people hear ‘it’s genetic’, what they think this means, is that their coding system has determined that they will suffer from a particular condition, and there is little to be done about it.

Luckily I’m pretty sure that isn’t how things like this work. Everything can change as a result of changing circumstances, including your genes. And the way you feel is constantly fluctuating.

Some are anxious in the middle of the night. Others are depressed first thing in the morning. Depression and anxiety can go from not existing, to being there, to becoming chronically bad, and then to completely disappearing again. Was it written in the code for it to happen that way? Of course not.

If you are physiologically sensitive to stress – if you were born with a particular biological weakness – it’s one thing to say this increases your susceptibility to so called mental disorders, and an altogether different thing to bring out the ‘it’s genetic’ mantra.

If genes determine your future, then you can’t be helped. But if brain and nervous system function gets influenced by the state of your metabolism (and vice versa), what you can do is work with the things that improve metabolic function (as well as brain function), and there are many. This changes the way prevention and treatment are able to be viewed.

There are different ways to work with weakness, and if you are given a reasonably accurate picture of biology, and you are willing to experiment, you can change your physiology or neurology over time, and significantly reduce your sensitivity to stress.

This doesn’t mean that you will be forever free from the harm of emotional or other kinds of stress and trauma. But it does mean that you can learn to improve how you manage stress, and avoid many exaggerated physiological responses which promote chronic illness.

Stress increases the demand for sugar, and when blood sugar runs low as a result of stressful events or under fueling, there are a whole lot of things that happen throughout the body in response to this, in an attempt to maintain reasonable function.

Stress and low blood sugar impact upon thyroid function and oxidative metabolism, and interference with these things, has a direct effect upon how fuel is used to provide energy for the brain and other systems.

When mitochondrial energy metabolism is suppressed, this can promote depression and anxiety, but how bad it is, and whether or not it becomes a chronic issue, depends on a lot of different things.

There is a powerful relationship between blood sugar dysregulation, and exposure to systemically rising levels of the stress substances, including cortisol, adrenaline, bacterial endotoxin, serotonin, estrogen, lactate, and nitric oxide.

It’s not by coincidence that these materials have been shown to play an important part in the suppression of oxidative energy metabolism, and in the promotion of mental dysregulation. They are some of the fundamental links between fuel issues and metabolic illness.

The polyunsaturated fats (PUFAs) are a big factor promoting ongoing biological issues. Stress and low fuel, promote the release of free fatty acids into the blood, in an attempt to provide an alternative fuel supply.

When fat circulating through the system is increasingly composed of PUFAs, this directly damages mitochondrial energy production, causes a further rise in stress hormone release, and increases the metabolically suppressive impact from exposure to the stress substances.

Interactions between the breakdown products of the PUFAs, the substances of stress, and excess iron, have also been shown to play a big part in causing the chronic inflammatory issues related to depression and anxiety, as well as to blood sugar, energy system, brain, and nervous system dysregulation.

Until it becomes commonplace to view the progression of disease states like diabetes, cancer, heart disease and dementia, as being linked with the development of chronic mood and other brain related issues – in large part because of the things that interfere with energy metabolism – it’s less likely that the significance of proper fueling, will be appreciated.

Even so, most people are aware of the connection between emotional distress and stomach issues. But how often do you hear people talking about the many ways this ties in with thyroid dysfunction, energy metabolism, and nervous system and brain dysfunction? Not very often.

When sugar is restricted, or when excess PUFAs, and other factors (such as protein or nutritional deficiencies), inhibit fuel usability, thyroid is interfered with, stress goes up, and digestive function is often impeded.

This can promote bacterial issues, as well as an increase in circulation into the main system, of many of the substances – like endotoxin, serotonin, estrogen, cortisol, and nitric oxide – which are able to encourage a chronic inflammatory state, potentially changing the way the body (and the brain and nervous system) responds to stress.

No organ in the body requires sugar for fuel more than the brain, and interference with the supply of fuel to the brain (and with the ability of the brain to properly use such fuel), can lead to serious consequences, including impairment of the perception of reality.

Again, I’m not saying that the trauma a person experiences is just a case of inappropriate perception requiring extra fuel. There is however, a big difference between feeling fearful or sad for a period of time (grieving a loss or facing a challenge), and suffering from the kind of chronic anxiety and depression, which can literally be there every day, without any understandable cause.

Evidence suggests that a hypometabolic state, resulting from exposure to ongoing stress, can be a driver of mental instability. It makes sense from a biological perspective. But when PUFAs and other stressful, inflammatory, energy metabolism interfering things, come into play, regulation of mood and other mind states, can go from fluctuating due to circumstances, to dysfunctional.

If you are exposed to chronically high levels of stress, this can create an energy system suppressed, inflamed, nervous system excited state, that becomes self feeding. And some are born with this state already in play.

But it isn’t written in stone. Many things either make the situation better or worse. If you can change something and get an improvement (and there is plenty of scientific evidence showing that you can), then you can get more improvement over time, and in a number of different ways. You just have to know some of the ways.

If you provide enough fuel (in the context of an appropriate diet), and if you remove as many of the things as possible, that prevent the proper use of fuel (and nutrition in general), the potential is there for greater healing, and improved biological function.

It doesn’t just come down to talk therapy and other stress reducing techniques, although they can certainly help to reduce nervous system excitation, improve energy systems, and protect against inefficient brain function, which can use up a great deal of energy unnecessarily.

But talk (and other) therapy isn’t enough in many cases, and popular ‘anti-depressants’ (and many related medications), often cause a worsening of metabolic and brain related issues.

It isn’t easy to reverse a lifetime of damage to metabolism, even when you have the right information, or the willingness to experiment. And lots of people give up if results take too long to come.

When someone recovers from depression, it’s often said that it mustn’t have been that serious, or it wasn’t a genetically driven case. When they don’t recover, it’s treatment-resistant, and it’s written in your genes. You’ll likely never hear, ‘oh, sorry, we just realized we’ve been doing the wrong things to help.’

I’m not a doctor or a scientist, and this isn’t intended as medical or psychiatric advice, but I’ve witnessed how the system explains and treats mental dysregulation issues, and it consistently fails to take advantage of large amounts of the best information available.

No scientific study is right about everything, providing all of the answers, but if you look at enough studies, you can extrapolate lots of good information, experiment, and join up many of the dots.

Sugar restriction is a dangerous tactic, because of the way that it simultaneously increases stress substance release, and suppresses thyroid and nervous system function, and oxidative energy metabolism.

Stressful experiences are real. Even so, the effects that they have on your brain, and emotions, and on health in general, don’t occur in isolation from metabolic function and energy production. In a sense, stress is a form of consumption.

Depression and anxiety are biological, metabolic, nervous system issues, and they are psychological, social and spiritual issues. Sometimes however, the more chronic and systemic the interference with metabolism and brain function is, the more of a difference improving fuel issues can make.

You can’t just slam on the fuel and always get immediate recovery. Inflammation, liver and digestive system damage, excess PUFAs and iron issues, nervous system sensitivity and other problems, all took time to develop, and can take time to improve.

Plenty of good quality sleep and daylight exposure, rest, and play, with a diet avoiding PUFAs, and limiting digestion interfering grains, nuts, beans, and under cooked vegetable matter, with enough protein and nutrients from milk, cheese, and gelatinous meats, and plenty of sugar from sweet fruits, fruit juice, white sugar, and honey, is one possible way to improve fueling, in order to help deal with stress related issues.

Some things which have been shown to help improve glucose utilization and energy production, include biotin, B6, thiamine, niacinamide and riboflavin, taurine, famotidine, cyproheptadine, aspirin, thyroid hormone, pregnenolone, progesterone, vitamin K, coconut oil, inosine, activated charcoal, red light, raw carrot, certain antibiotics, methylene blue, and numerous other pro-metabolism things.

Some people have metabolic energy system related issues, and don’t suffer from mental dysregulation. Hereditary, psychosocial, and environmental factors, play their part here, but this is not to say that their health and happiness can’t be improved at all.

For those who are unable to figure out a way around depression or anxiety, my experience (including that of many I have listened to and learned from), has shown me that much can be gained from a look at fuel issues, in the context of a pro-metabolic, stress reducing diet and lifestyle.

It’s very common now, for sugar to be viewed as an ‘addictive’ substance, masking pain (in the way that some substances do), rather than what it is: optimal fuel for metabolic function, required in varying quantities, depending on stress levels and strength of metabolism, but always required. Either you provide it, or the body will find another more costly way.

There are lots of studies below. Read some of them if you want further information. I don’t necessarily agree with every word in every study included, and nor should anyone probably, but they are related either directly or indirectly.

See More Here

Psychosom Med. 2010 May;72(4):357-64. Low Calorie Dieting Increases Cortisol. Tomiyama AJ, Mann T, Vinas D, Hunger JM, Dejager J, Taylor SE.

Biogerontology. 2012 Apr;13(2):93-103. High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse. Honma T, Shinohara N, Ito J, Kijima R, Sugawara S, Arai T, Tsuduki T, Ikeda I.

Am J Med. 1986 Aug;81(2):280-4. Sucrose substitution in prevention and reversal of the fall in metabolic rate accompanying hypocaloric diets. Hendler RG, Walesky M, Sherwin RS.

Am J Physiol Cell Physiol. 2006 May;290(5):C1321-33. Polyunsaturated fatty acids mobilize intracellular Ca2+ in NT2 human teratocarcinoma cells by causing release of Ca2+ from mitochondria. Zhang BX, Ma X, Zhang W, Yeh CK, Lin A, Luo J, Sprague EA, Swerdlow RH, Katz MS.

J Neuroendocrinol. 2001 Sep;13(9):827-35. Review. A new perspective on glucocorticoid feedback: relation to stress, carbohydrate feeding and feeling better. Laugero KD.

Am J Primatol. 2010 Jun;72(7):600-6. Sources of variation in fecal cortisol levels in howler monkeys in Belize. Behie AM, Pavelka MS, Chapman CA.

Case Rep Psychiatry. 2016;2016:7165425. Generalized Anxiety Disorder and Hypoglycemia Symptoms Improved with Diet Modification. Aucoin M, Bhardwaj S.

Am J Clin Nutr. 2010 Apr;91(4):940-9. Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression. Ghanim H, Sia CL, Upadhyay M, Korzeniewski K, Viswanathan P, Abuaysheh S, Mohanty P, Dandona P.

Diabetes Metab. 2005 Apr;31(2):178-88. Consumption of carbohydrate solutions enhances energy intake without increased body weight and impaired insulin action in rat skeletal muscles. Ruzzin J, Lai YC, Jensen J.

Front Endocrinol (Lausanne). 2015 Nov 20;6:175. Recurrent Hypoglycemia Increases Anxiety and Amygdala Norepinephrine Release During Subsequent Hypoglycemia. McNay E.

J Clin Endocrinol Metab. 2000 Dec;85(12):4515-9. Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults. Moore MC, Cherrington AD, Mann SL, Davis SN.

Diabetes Care. 2001 Nov;24(11):1882-7. Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes. Moore MC, Davis SN, Mann SL, Cherrington AD.

BMC Medicine volume 13, Article number: 68 (2015). The many roads to mitochondrial dysfunction in neuroimmune and neuropsychiatric disorders. Gerwyn Morris & Michael Berk.

Neurosci Biobehav Rev. 2015 Apr;51:164-88. Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant. Andrews PW, Bharwani A, Lee KR, Fox M, Thomson JA Jr.

ACS Chem Neurosci. 2014 Oct 15;5(10):908-19. Mice Genetically Depleted of Brain Serotonin Do Not Display a Depression-like Behavioral Phenotype. Angoa-Pérez M, Kane MJ, Briggs DI, Herrera-Mundo N, Sykes CE, Francescutti DM, Kuhn DM.

Proc Natl Acad Sci U S A. 2015 Mar 17;112(11):3463-8. Insulin resistance in brain alters dopamine turnover and causes behavioral disorders. Kleinridders A, Cai W, Cappellucci L, Ghazarian A, Collins WR, Vienberg SG, Pothos EN, Kahn CR.

Curr Alzheimer Res. 2016;13(5):475-86. Hypometabolism in Brain of Cognitively Normal Patients with Depressive Symptoms is Accompanied by Atrophy-Related Partial Volume Effects. Brendel M, Reinisch V, Kalinowski E, Levin J, Delker A, Därr S, Pogarell O, Förster S, Bartenstein P, Rominger A, Alzheimer’s Disease Neuroimaging Initiative.

J R Soc Interface. 2016 Sep;13(122). pii: 20160539. Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide. Pretorius E, Mbotwe S, Bester J, Robinson CJ, Kell DB.

Crit Care Med. 2008 Oct;36(10):2726-33. Intensive Care Unit Hypoglycemia Predicts Depression during Early Recovery from Acute Lung Injury. Dowdy DW, Dinglas V, Mendez-Tellez PA, Bienvenu OJ, Sevransky J, Dennison CR, Shanholtz C, Needham DM.

J Clin Psychiatry. 2015 Dec;76(12):1658-67. Oxidative Stress and Antioxidant Parameters in Patients With Major Depressive Disorder Compared to Healthy Controls Before and After Antidepressant Treatment: Results From a Meta-Analysis. Jiménez-Fernández S, Gurpegui M, Díaz-Atienza F, Pérez-Costillas L, Gerstenberg M, Correll CU.

Neuropsychopharmacology. 2014 Nov;39(12):2867-73. A Randomized, Double-Blind, Placebo-Controlled Trial of Pregnenolone for Bipolar Depression. Brown ES, Park J, Marx CE, Hynan LS, Gardner C, Davila D, Nakamura A, Sunderajan P, Lo A, Holmes T.

Exp Clin Psychopharmacol. 2010 Feb;18(1):78-86. Effects of acute progesterone administration upon responses to acute psychosocial stress in men. Childs E, Van Dam NT, de Wit H.

The Journal of Clinical Endocrinology & Metabolism, Volume 38, Issue 5, 1 May 1974, Pages 836–840, Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine. JAMES W. PLONK, CARL H. BIVENS, JEROME M. FELDMAN.

Nat Clin Pract Endocrinol Metab. 2008 Feb;4(2):91-101. Drug insight: selective agonists and antagonists of the glucocorticoid receptor. McMaster A, Ray DW.

Ann Neurol. 1990 Jul;28(1):57-64. Selective hypometabolism in the inferior frontal lobe in depressed patients with Parkinson’s disease. Mayberg HS, Starkstein SE, Sadzot B, Preziosi T, Andrezejewski PL, Dannals RF, Wagner HN Jr, Robinson RG.

J Clin Invest. 2017 Apr 3;127(4):1370-1374. Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain. Anand Kumar Singh, Joanna Zajdel, Elahe Mirrasekhian, Nader Almoosawi, Isabell Frisch, Anna M. Klawonn, Maarit Jaarola, Michael Fritz, and David Engblom

Acta Physiol (Oxf). 2017 Feb;219(2):409-440. Hypometabolism as the ultimate defence in stress response: how the comparative approach helps understanding of medically relevant questions. Gorr TA.

J Diabetes. 2015 Nov;7(6):800-8. Depression in Chinese patients with type 2 diabetes: associations with hyperglycemia, hypoglycemia, and poor treatment adherence. Zhang Y, Ting RZ, Yang W, Jia W, Li W, Ji L, Guo X, Kong AP, Wing YK, Luk AO, Sartorius N, Morisky DE, Oldenburg B, Weng J, Chan JC;

Metabolism. 2012 Feb;61(2):229-36. Acute hypoglycemia causes depressive-like behaviors in mice. Park MJ, Yoo SW, Choe BS, Dantzer R, Freund GG.

Nat Med. 2013 Jun;19(6):773-7. Astrocyte-derived ATP modulates depressive-like behaviors. Cao X, Li LP, Wang Q, Wu Q, Hu HH, Zhang M, Fang YY, Zhang J, Li SJ, Xiong WC, Yan HC, Gao YB, Liu JH, Li XW, Sun LR, Zeng YN, Zhu XH, Gao TM.

Clin Exp Pharmacol Physiol. 2016 Dec;43(12):1208-1215. Beneficial effect of aspirin against interferon-α-2b – induced depressive behavior in Sprague Dawley rats. Bhatt S, Pundarikakshudu K, Patel P, Patel N, Panchal A, Shah G, Goswami S.

Nature. 2016 Sep 1;537(7618):97-101. Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala. Marcinkiewcz CA, Mazzone CM, D’Agostino G, Halladay LR, Hardaway JA, DiBerto JF, Navarro M, Burnham N, Cristiano C, Dorrier CE, Tipton GJ, Ramakrishnan C, Kozicz T, Deisseroth K, Thiele TE, McElligott ZA, Holmes A, Heisler LK, Kash TL.

Neuropsychopharmacology volume 43, pages459–468(2018). Decreased Brain pH as a Shared Endophenotype of Psychiatric Disorders. Hideo Hagihara, Vibeke S Catts, Yuta Katayama, Hirotaka Shoji, Tsuyoshi Takagi, Freesia L Huang, Akito Nakao, Yasuo Mori, Kuo-Ping Huang, Shunsuke Ishii, Isabella A Graef, Keiichi I Nakayama, Cynthia Shannon Weickert & Tsuyoshi Miyakawa.

Diabetes. 2005 Jul;54(7):1926-33. A High-Fat Diet Coordinately Downregulates Genes Required for Mitochondrial Oxidative Phosphorylation in Skeletal Muscle. Lauren M. Sparks, Hui Xie, Robert A. Koza, Randall Mynatt, Matthew W. Hulver, George A. Bray and Steven R. Smith.

BMC Psychiatry volume 17, Article number: 150 (2017). A case of recurrent depressive disorder presenting with Alice in Wonderland syndrome: psychopathology and pre- and post-treatment FDG-PET findings. Tatsushi Yokoyama, Tsuyoshi Okamura, Miwako Takahashi, Toshimitsu Momose & Shinsuke Kondo.

Pharmacol Rep. 2010 Nov-Dec;62(6):1030-40. Effects of neurosteroids on the human corticotropin-releasing hormone gene. Budziszewska B, Zając A, Basta-Kaim A, Leśkiewicz M, Steczkowska M, Lasoń W, Kaciński M.

Psychogeriatrics. 2016 Nov;16(6):376-381. Reversal of cerebral glucose hypometabolism on positron emission tomography with electroconvulsive therapy in an elderly patient with a psychotic episode. Hassamal S, Jolles P, Pandurangi A.

Curr Neuropharmacol. 2014 Mar;12(2):108-19. Novel Therapeutic Targets in Depression and Anxiety: Antioxidants as a Candidate Treatment. Xu Y, Wang C, Klabnik JJ, O’Donnell JM.

Can J Psychiatry. 1994 Feb;39(1):8-11. Iron overload and psychiatric illness. Cutler P.

J Nutr Biochem. 2013 Sep;24(9):1634-44. Effects of excess dietary iron and fat on glucose and lipid metabolism. Choi JS, Koh IU, Lee HJ, Kim WH, Song J.

Neurology. 2017 May 9;88(19):1814-1821. Neuropsychiatric symptoms predict hypometabolism in preclinical Alzheimer disease. Ng KP, Pascoal TA, Mathotaarachchi S, Chung CO, Benedet AL, Shin M, Kang MS, Li X, Ba M, Kandiah N, Rosa-Neto P, Gauthier S; Alzheimer’s Disease Neuroimaging Initiative.

Sci Rep. 2017 Sep 7;7(1):10776. Gender-based differences in host behavior and gut microbiota composition in response to high fat diet and stress in a mouse model. Bridgewater LC, Zhang C, Wu Y, Hu W, Zhang Q, Wang J, Li S, Zhao L.

BMJ Open Diabetes Res Care. 2015 May 16;3(1):e000063. Association of severe hypoglycemia with depressive symptoms in patients with type 2 diabetes: the Fukuoka Diabetes Registry. Kikuchi Y, Iwase M, Fujii H, Ohkuma T, Kaizu S, Ide H, Jodai T, Idewaki Y, Nakamura U, Kitazono T.

Mol Psychiatry. 2009 May;14(5):537-45. Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study. Maddock RJ, Buonocore MH, Copeland LE, Richards AL.

Psychiatry Res. 2017 Apr;250:113-120. Insulin resistance, atherogenicity, and iron metabolism in multiple sclerosis with and without depression: Associations with inflammatory and oxidative stress biomarkers and uric acid. Oliveira SR, Kallaur AP, Lopes J, Colado Simão AN, Reiche EM, de Almeida ERD, Morimoto HK, de Carvalho Jennings de Pereira WL, Alfieri DF, Flauzino T, de Meleck Proença C, Gomes AM, Kaimen-Maciel DR, Maes M.

Diabetes. 2011 Jan;60(1):80-7. Iron Overload and Diabetes Risk: A Shift From Glucose to Fatty Acid Oxidation and Increased Hepatic Glucose Production in a Mouse Model of Hereditary Hemochromatosis. Huang J, Jones D, Luo B, Sanderson M, Soto J, Abel ED, Cooksey RC, McClain DA.

Mol Psychiatry. 2016 Nov;21(11):1599-1607. Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features. Heidari M, Johnstone DM, Bassett B, Graham RM, Chua AC, House MJ, Collingwood JF, Bettencourt C, Houlden H, Ryten M, Olynyk JK, Trinder D, Milward EA.

Mol Neurobiol. 2016 Dec;53(10):7351-7362. The effect of chronic tianeptine administration on the brain mitochondria: direct links with an animal model of depression. Głombik K, Stachowicz A, Olszanecki R, Ślusarczyk J, Trojan E, Lasoń W, Kubera M, Budziszewska B, Spedding M, Basta-Kaim A.

J Clin Psychopharmacol. 2017 Feb;37(1):40-45. Increased Brain Lactate During Depressive Episodes and Reversal Effects by Lithium Monotherapy in Drug-Naive Bipolar Disorder: A 3-T 1H-MRS Study. Machado-Vieira R, Zanetti MV, Otaduy MC, De Sousa RT, Soeiro-de-Souza MG, Costa AC, Carvalho AF, Leite CC, Busatto GF, Zarate CA Jr, Gattaz WF.

Mol Psychiatry. 2016 Oct;21(10):1358-65. Inflammation is associated with decreased functional connectivity within corticostriatal reward circuitry in depression. Felger JC, Li Z, Haroon E, Woolwine BJ, Jung MY, Hu X, Miller AH.

PLoS One. 2015 Oct 7;10(10):e0138904. A Meta-Analysis of Oxidative Stress Markers in Depression. Liu T, Zhong S, Liao X, Chen J, He T, Lai S, Jia Y.

Trends Neurosci. 2013 Oct;36(10):587-97. Sugar for the brain: the role of glucose in physiological and pathological brain function. Mergenthaler P, Lindauer U, Dienel GA, Meisel A.

Proc Natl Acad Sci U S A. 2015 Mar 17;112(11):3463-8. Insulin resistance in brain alters dopamine turnover and causes behavioral disorders. Kleinridders A, Cai W, Cappellucci L, Ghazarian A, Collins WR, Vienberg SG, Pothos EN, Kahn CR.

Neuropsychiatr Dis Treat. 2013;9:567-73. Mitochondrial dysfunction, oxidative stress, and major depressive disorder. Tobe EH.

Ann Fam Med. 2013 May-Jun;11(3):245-50. Association of Depression With Increased Risk of Severe Hypoglycemic Episodes in Patients With Diabetes. Katon WJ, Young BA, Russo J, Lin EH, Ciechanowski P, Ludman EJ, Von Korff MR.

Indian J Psychol Med. 2017 May-Jun;39(3):342-346. Comparative study of psychiatric manifestations among Type I and Type II diabetic patients. Chaudhary R, Kumar P, Chopra A, Chabbra S, Singh P.

Neuropharmacology. 2012 Jan;62(1):485-91. Inhibition of iNOS induces antidepressant-like effects in mice: pharmacological and genetic evidence. Montezuma K, Biojone C, Lisboa SF, Cunha FQ, Guimarães FS, Joca SR.

J Affect Disord. 2001 Mar;63(1-3):221-4. Elevated plasma nitrate levels in depressive states. Suzuki E, Yagi G, Nakaki T, Kanba S, Asai M.

Redox Rep. 2014 Mar;19(2):92-6. Lipid peroxidation markers in children with anxiety disorders and their diagnostic implications. Ceylan MF, Guney E, Alisik M, Ergin M, Dinc GS, Goker Z, Eker S, Kizilgun M, Erel O.

J Affect Disord. 2011 Mar;129(1-3):175-82. Association between inducible and neuronal nitric oxide synthase polymorphisms and recurrent depressive disorder. Gałecki P, Maes M, Florkowski A, Lewiński A, Gałecka E, Bieńkiewicz M, Szemraj J.

Neuropsychobiology. 2003;47(1):31-6. Influence of mirtazapine on salivary cortisol in depressed patients. Laakmann G, Hennig J, Baghai T, Schüle C.

Biol Sex Differ. 2018 Jan 19;9(1):7. Effects of gut-derived endotoxin on anxiety-like and repetitive behaviors in male and female mice. Fields CT, Chassaing B, Castillo-Ruiz A, Osan R, Gewirtz AT, de Vries GJ.

Metab Brain Dis. 2013 Mar;28(1):93-105. Treatment with tianeptine induces antidepressive-like effects and alters the neurotrophin levels, mitochondrial respiratory chain and cycle Krebs enzymes in the brain of maternally deprived adult rats. Della FP, Abelaira HM, Réus GZ, Santos MA, Tomaz DB, Antunes AR, Scaini G, Morais MO, Streck EL, Quevedo J.

JAMA Psychiatry. 2015 Aug;72(8):794-802. Serotonin Synthesis and Reuptake in Social Anxiety Disorder. Frick A, Åhs F, Engman J, Jonasson M, Alaie I, Björkstrand J, Frans Ö, Faria V, Linnman C, Appel L, Wahlstedt K, Lubberink M, Fredrikson M, Furmark T.

Rev Bras Ginecol Obstet. 2010 Jul;32(7):321-6. [Depression and anxiety symptoms in hypothyroid women]. Andrade Junior NE, Pires ML, Thuler LC.

Behav Brain Res. 2015 Jan 1;276:111-7. Endotoxaemia resulting from decreased serotonin tranporter (5-HTT) function: a reciprocal risk factor for depression and insulin resistance? Pomytkin IA, Cline BH, Anthony DC, Steinbusch HW, Lesch KP, Strekalova T.

J Clin Diagn Res. 2014 Dec;8(12):CC04-7. Oxidative Stress and Major Depression. Bajpai A, Verma AK, Srivastava M, Srivastava R.

Inflamm Intest Dis. 2016 Oct;1(3):135-145. Increased Intestinal Permeability and Decreased Barrier Function: Does It Really Influence the Risk of Inflammation? Fukui H.

Front Neurosci. 2017 Sep 7;11:493. The Energy Metabolism Dysfunction in Psychiatric Disorders Postmortem Brains: Focus on Proteomic Evidence. Zuccoli GS, Saia-Cereda VM, Nascimento JM, Martins-de-Souza D.

Horm Metab Res. 2004 Sep;36(9):650-3. Depression and anxiety in different thyroid function states. Larisch R, Kley K, Nikolaus S, Sitte W, Franz M, Hautzel H, Tress W, Müller HW.

Elevated morning cortisol is a stratified population-level biomarker for major depression in boys only with high depressive symptoms. Matthew Owens, Joe Herbert, Peter B. Jones, Barbara J. Sahakian, Paul O. Wilkinson, Valerie J. Dunn, Timothy J. Croudace, and Ian M. Goodyer

Scientific Reports volume 7, Article number: 43192 (2017). Decreased Glycogen Content Might Contribute to Chronic Stress-Induced Atrophy of Hippocampal Astrocyte volume and Depression-like Behavior in Rats. Yunan Zhao, Qiang Zhang, Xiao Shao, Liufeng Ouyang, Xin Wang, Kexuan Zhu & Lin Chen.

J Neuroinflammation. 2012 Jul 6;9:75. Inducible nitric oxide synthase is involved in the modulation of depressive behaviors induced by unpredictable chronic mild stress. Peng YL, Liu YN, Liu L, Wang X, Jiang CL, Wang YX.

Behav Brain Res. 2017 Mar 30;322(Pt A):70-82. Inhibition of iNOS alleviates cognitive deficits and depression in diabetic mice through downregulating the NO/sGC/cGMP/PKG signal pathway. Zhou XY, Zhang F, Ying CJ, Chen J, Chen L, Dong J, Shi Y, Tang M, Hu XT, Pan ZH, Xu NN, Zheng KY, Tang RX, Song YJ.

Qual Life Res. 2006 May;15(4):695-703. Health-related Quality of Life, Depression and Anxiety in Thyroid Cancer Patients. Tagay S, Herpertz S, Langkafel M, Erim Y, Bockisch A, Senf W, Görges R.

Diabetes Care. 2014 Nov;37(11):3076-83. Brain Iron Overload, Insulin Resistance, and Cognitive Performance in Obese Subjects: A Preliminary MRI Case-Control Study. Blasco G, Puig J, Daunis-I-Estadella J, Molina X, Xifra G, Fernández-Aranda F, Pedraza S, Ricart W, Portero-Otín M, Fernández-Real JM.

Intelligence, Volume 66, 2018, p. 1, High intelligence: A risk factor for psychological and physiological overexcitabilities. Ruth I.Karpinski Audrey M. Kinase Kolb Nicole A.Tetreault Thomas B.Borowski.

Proc Natl Acad Sci U S A. 2015 Dec 15;112(50):15486-91. Mitochondrial function in the brain links anxiety with social subordination. Hollis F, van der Kooij MA, Zanoletti O, Lozano L, Cantó C, Sandi C.

Endocr J. 2004 Jun;51(3):311-5. Assessment of Anxiety in Subclinical Thyroid Disorders. Sait Gönen M, Kisakol G, Savas Cilli A, Dikbas O, Gungor K, Inal A, Kaya A.

Emory University, Atlanta, GA, United States, Glial Cell Glycogen and Stress-induced Depression. Bonsall, Robert W.

Diabetes. 2005 Jul;54(7):1926-33. A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle. Sparks LM, Xie H, Koza RA, Mynatt R, Hulver MW, Bray GA, Smith SR.

Thyroid Research and Practice 2018, Volume 15, Issue 1, Page 10-14. Depression, anxiety, and somatization in patients with clinical and subclinical hypothyroidism: An exploratory study. Kavita Sanjiv Kale, Bharati Baviskar.

Proceedings of the National Academy of Sciences 111(34) August 2014, Socially responsive effects of brain oxidative metabolism on aggression. Hongmei Li-Byarlay, Clare C. Rittschof, Jonathan H. Massey, Barry R. Pittendrigh, and Gene E. Robinson

Pharmacol Rep. 2010 Nov-Dec;62(6):1030-40. Effects of neurosteroids on the human corticotropin-releasing hormone gene. Budziszewska B, Zając A, Basta-Kaim A, Leśkiewicz M, Steczkowska M, Lasoń W, Kaciński M.

Nutrients. 2015 Jul 23;7(8):6055-72. Higher Body Iron Is Associated with Greater Depression Symptoms among Young Adult Men but not Women: Observational Data from the Daily Life Study. Richardson AC, Heath AL, Haszard JJ, Polak MA, Houghton LA, Conner TS.

Neuropsychiatr Dis Treat. 2015 Sep 29;11:2479-91. A meta-analysis of lipid peroxidation markers in major depression. Mazereeuw G, Herrmann N, Andreazza AC, Khan MM, Lanctôt KL.

Indian J Endocrinol Metab. 2016 Jul-Aug;20(4):468-74. Prevalence of anxiety and depressive symptoms among patients with hypothyroidism. Bathla M, Singh M, Relan P.

J Neurochem. 2004 May;89(3):537-52. Brain glycogen re-awakened. Angus M. Brown.

Mitochondrion. 2011 Jan;11(1):89-96. Improvement of mitochondrial energy and oxidative balance during intestinal differentiation. Santandreu FM, Oliver J, Roca P.

Am J Psychiatry. 2017 Jan 1;174(1):42-50. Neurometabolic Disorders: Potentially Treatable Abnormalities in Patients With Treatment-Refractory Depression and Suicidal Behavior. Pan LA, Martin P, Zimmer T, Segreti AM, Kassiff S, McKain BW, Baca CA, Rengasamy M, Hyland K, Walano N, Steinfeld R, Hughes M, Dobrowolski SK, Pasquino M, Diler R, Perel J, Finegold DN, Peters DG, Naviaux RK, Brent DA, Vockley J.

Sci Rep. 2014 Feb 26;4:4199. Oral administration of inosine produces antidepressant-like effects in mice. Muto J, Lee H, Lee H, Uwaya A, Park J, Nakajima S, Nagata K, Ohno M, Ohsawa I, Mikami T.

Front Neuroenergetics. 2012 Mar 2;4:3. Brain glycogen—new perspectives on its metabolic function and regulation at the subcellular level. Obel LF, Müller MS, Walls AB, Sickmann HM, Bak LK, Waagepetersen HS, Schousboe A.

Psychiatry Investig. 2010 Sep;7(3):208-14. Frontal Dysfunction Underlies Depression in Mild Cognitive Impairment: A FDG-PET Study. Lee HS, Choo IH, Lee DY, Kim JW, Seo EH, Kim SG, Park SY, Shin JH, Kim KW, Woo JI.

#sugarblaming
#sugarfeedsthyroid
#pufaispoison
#raypeat

Image: nalakagunawardene.com

You may also like...

2 Responses

  1. Are you tired of running on empty? Are you sick and tired or being sick and tired? It’s time to fuel up. It’s time to get some R.E.S.T.

  2. Avatar Jay says:

    This article is my experience for the last 20 years. Chronic anxiety that will last as long as the the job stress remains so it was a consistent 1 year once at an unusually high level most of the time. Generalized Anxiety Disorder is not normal stress I keep telling family. This is what eventually led to Dr. Ray Peat’s ideas and cowseatgrass. The diet change is opposite of what med est. recommends in many ways but I have a marked improvement. SSRI’s just worsened the condition making the experience even more maddening. A valium plus diet has made all the different for what’s worth. Valium drug Diazapem is out of patent so no wonder my doctors never recommended it. Thanks Dan for passing on valuable info!

Leave a Reply

Your email address will not be published. Required fields are marked *

x
Please "like" us:Already liked? You can close this
Secured By miniOrange