Are You Running On Empty?

What if I said to you that chronic anxiety and depression are metabolic issues, that one way or another they relate to fuel, and that it cannot really be any other way.

No, I’m not saying you can simply consume more sugar (fuel) and then all your problems will miraculously go away, but it certainly isn’t too far from the truth. You need sugar for fuel, you need fuel for energy, and you need energy for protection against stress.

Mood dysregulation is a product of stress. When stress exceeds or interferes with energy supply, a whole lot of metabolically problematic things start to happen. Whether this leads to chronic issues depends on a variety of factors.

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.

In reality – no matter which angle you choose to look at it from – it eventually comes down to the degree and kind of stress a person is (and has been) exposed to, and the way in which that stress is able to be met, metabolically speaking.

To put it another way, many things are stressful, but how you’re able to deal with or recover from stress (in a biological sense), will always be related to metabolism and energy production. In some cases, a small stress can have a big impact, in other cases a big stress can be easily handled.

I’m not saying the kinds of experiences a person has aren’t relevant. They are. But there is a difference between the impact of emotionally stressful or traumatic situations, when metabolism is fueled and functioning well, compared to when it isn’t.

Emotional stress has a powerful impact. You can immediately notice what it does to digestion, sleep, anxiety, mood, skin and other things. You can also observe how changing the way you perceive a situation changes the way your body responds. Biology influences psychology and vice versa.

All this relates to energy system function. When you interfere with metabolism it has an effect. How it can effect the way you interpret and feel about the outside world, is influenced by a number of physiological circumstances. When metabolic function is damaged, this more easily becomes a downward spiraling vicious circle.

So how to fix it? If you’re after a black and white, ‘it’s your genes’ kind of solution, I’m afraid I don’t have that for you. And that never really turns out to be a solution anyway. More likely just a diversion.

It’s true that hereditary factors make a person either more or less susceptible to the negative effects of stress, however the argument that things like depression simply come down to genetics seems to me to be misleading. Unless when you say ‘genetics’, what you mean is biology. In which case yes, that’s closer to the truth.

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. In reality, everything can change as a result of changing circumstances, including your genes. 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. 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 mood disorders, and an altogether different thing to bring out the ‘it’s genetic’ mantra.

If genes actually determined your future, then you can’t really be helped. But if mood is influenced by the state of your metabolism, what you can do is work with the things that improve metabolic function, and there are many. It might seem to some like semantics, but it changes the way prevention and treatment are able to be viewed.

There are many different ways to work with weakness, and if you have a decent understanding of biology, and you are willing to experiment, you can change your physiology over time, and significantly reduce your sensitivity to stress.

This doesn’t mean that you will be forever free from the potentially negative effects of emotional or other kinds of stress. At the very least though, it does mean that you can learn to manage stress better, and avoid many exaggerated physiological responses which can lead to 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.

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 stress substances including cortisol, adrenalin, 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 mood dysregulation. They are some of the fundamental links between fuel issues and metabolic illness.

The polyunsaturated fats (PUFAs) are a big factor promoting chronic issues in this regard. 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 PUFA, 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 PUFA, 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 and energy 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 issues – largely because of the things that interfere with energy metabolism – it’s less likely that the significance of interference with proper fueling, will be appreciated.

Even so, most people are acutely 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 and energy metabolism?

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

This promotes bacterial issues, and an increase in circulation into the main system, of many of the substances – like endotoxin, serotonin, estrogen, cortisol and nitric oxide – which encourage a chronic inflammatory state, potentially changing the way the body (including the brain) 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, drives mood instability. It makes a lot of sense from a biological perspective. But when PUFA and other stressful, inflammatory, energy metabolism interfering things come into play, regulation of mood can go from fluctuating due to circumstances, to dysfunctional.

If you are exposed to chronically high levels of stress, you can create a kind of energy system suppressed, inflamed, nervous system excited state, that becomes self feeding. You can also be born with this kind of state already in play.

But it isn’t written in stone. Many things are either making the situation better or worse. If you can change something and get an improvement (and there is plenty of evidence just in the science alone which shows 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, the potential is there for significant healing and biological change.

It doesn’t just come down to talk therapy and other stress reducing techniques, although they can certainly help to reduce nervous system excitation, limit interference with energy systems, and decrease excessive brain use, which likely wastes as much energy as anything.

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

And it isn’t easy to reverse the effects of a lifetime of damage to metabolism, regardless of the fact that many do not have the right information available to them, or the willingness to experiment. People often give up if results take too long to come.

When a person recovers from depression, it is 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 this all wrong.’

I’m not a doctor or a scientist, but I’ve witnessed how the medical system explains and treats mood related issues, and it seems to me to consistently fall short of taking advantage of the biological information available.

Perhaps it’s true that no scientific study can be right about everything, providing all of the answers, but if you look at enough studies you can extrapolate information, experiment, and join up the dots.

Sugar restriction is a dangerous tactic because of the way that it can simultaneously increase stress substance release, and suppress thyroid function and oxidative energy metabolism.

Stressful experiences are very real. Even so, the effects that they have on your brain and your emotions, and on your health in general, do not happen in isolation from metabolic function and energy production. In a sense, stress is another form of consumption.

Chronic depression and anxiety are as much biological, metabolic issues, as they are psychological or social issues. The more chronic and systemic the interference with metabolism is, the more of a difference improving fuel issues can make.

No you can’t necessarily just slam on the fuel and get immediate recovery. Inflammation, liver and digestive system damage, excess PUFA and iron storage, nervous system sensitivity and other issues took time to develop, and take time to change.

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

Some other 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 pro-metabolism things.

There are those who have metabolic energy system related issues who never suffer from chronic mood dysregulation. Hereditary, psychosocial and environmental factors play their part here, but this is not to say that health and happiness can not be improved in these cases too.

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

It’s increasingly common for sugar to be viewed as an ‘addictive’ substance, masking pain (in the way that some substances do), rather than what it really 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 many 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.

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Low Calorie Dieting Increases Cortisol

High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse.

Sucrose substitution in prevention and reversal of the fall in metabolic rate accompanying hypocaloric diets.

Polyunsaturated fatty acids mobilize intracellular Ca2+ in NT2 human teratocarcinoma cells by causing release of Ca2+ from mitochondria.

A new perspective on glucocorticoid feedback: relation to stress, carbohydrate feeding and feeling better.

Sources of variation in fecal cortisol levels in howler monkeys in Belize.

Generalized Anxiety Disorder and Hypoglycemia Symptoms Improved with Diet Modification

Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression.

Consumption of carbohydrate solutions enhances energy intake without increased body weight and impaired insulin action in rat skeletal muscles.

Recurrent Hypoglycemia Increases Anxiety and Amygdala Norepinephrine Release During Subsequent Hypoglycemia

Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults.

Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes.

The many roads to mitochondrial dysfunction in neuroimmune and neuropsychiatric disorders

Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant

Mice Genetically Depleted of Brain Serotonin Do Not Display a Depression-like Behavioral Phenotype

Insulin resistance in brain alters dopamine turnover and causes behavioral disorders

Hypometabolism in Brain of Cognitively Normal Patients with Depressive Symptoms is Accompanied by Atrophy-Related Partial Volume Effects.

Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide

Intensive Care Unit Hypoglycemia Predicts Depression during Early Recovery from Acute Lung Injury

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

A Randomized, Double-Blind, Placebo-Controlled Trial of Pregnenolone for Bipolar Depression

Effects of acute progesterone administration upon responses to acute psychosocial stress in men

Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine

Drug insight: selective agonists and antagonists of the glucocorticoid receptor.

Selective hypometabolism in the inferior frontal lobe in depressed patients with Parkinson’s disease.

Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain

Hypometabolism as the ultimate defence in stress response: how the comparative approach helps understanding of medically relevant questions.

Depression in Chinese patients with type 2 diabetes: associations with hyperglycemia, hypoglycemia, and poor treatment adherence

Acute hypoglycemia causes depressive-like behaviors in mice

Astrocyte-derived ATP modulates depressive-like behaviors.

Beneficial effect of aspirin against interferon-α-2b – induced depressive behavior in Sprague Dawley rats

Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala

Decreased Brain pH as a Shared Endophenotype of Psychiatric Disorders

A High-Fat Diet Coordinately Downregulates Genes Required for Mitochondrial Oxidative Phosphorylation in Skeletal Muscle

A case of recurrent depressive disorder presenting with Alice in Wonderland syndrome: psychopathology and pre- and post-treatment FDG-PET findings

Effects of neurosteroids on the human corticotropin-releasing hormone gene.

Reversal of cerebral glucose hypometabolism on positron emission tomography with electroconvulsive therapy in an elderly patient with a psychotic episode.

Novel Therapeutic Targets in Depression and Anxiety: Antioxidants as a Candidate Treatment

Iron overload and psychiatric illness.

Effects of excess dietary iron and fat on glucose and lipid metabolism.

Neuropsychiatric symptoms predict hypometabolism in preclinical Alzheimer disease

Gender-based differences in host behavior and gut microbiota composition in response to high fat diet and stress in a mouse model

Association of severe hypoglycemia with depressive symptoms in patients with type 2 diabetes: the Fukuoka Diabetes Registry

Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study

Insulin resistance, atherogenicity, and iron metabolism in multiple sclerosis with and without depression: Associations with inflammatory and oxidative stress biomarkers and uric acid.

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

Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features

The effect of chronic tianeptine administration on the brain mitochondria: direct links with an animal model of depression

Increased Brain Lactate During Depressive Episodes and Reversal Effects by Lithium Monotherapy in Drug-Naive Bipolar Disorder: A 3-T 1H-MRS Study

Inflammation is associated with decreased functional connectivity within corticostriatal reward circuitry in depression

A Meta-Analysis of Oxidative Stress Markers in Depression

Sugar for the brain: the role of glucose in physiological and pathological brain function

Insulin resistance in brain alters dopamine turnover and causes behavioral disorders.

Mitochondrial dysfunction, oxidative stress, and major depressive disorder

Association of Depression With Increased Risk of Severe Hypoglycemic Episodes in Patients With Diabetes

Comparative study of psychiatric manifestations among Type I and Type II diabetic patients

Inhibition of iNOS induces antidepressant-like effects in mice: pharmacological and genetic evidence.

Elevated plasma nitrate levels in depressive states.

Lipid peroxidation markers in children with anxiety disorders and their diagnostic implications

Association between inducible and neuronal nitric oxide synthase polymorphisms and recurrent depressive disorder.

Influence of mirtazapine on salivary cortisol in depressed patients.

Effects of gut-derived endotoxin on anxiety-like and repetitive behaviors in male and female mice.

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.

Serotonin Synthesis and Reuptake in Social Anxiety Disorder

[Depression and anxiety symptoms in hypothyroid women].

Endotoxaemia resulting from decreased serotonin tranporter (5-HTT) function: a reciprocal risk factor for depression and insulin resistance?

Oxidative Stress and Major Depression

Increased Intestinal Permeability and Decreased Barrier Function: Does It Really Influence the Risk of Inflammation?

The Energy Metabolism Dysfunction in Psychiatric Disorders Postmortem Brains: Focus on Proteomic Evidence

Depression and anxiety in different thyroid function states.

Elevated morning cortisol is a stratified population-level biomarker for major depression in boys only with high depressive symptoms

Decreased Glycogen Content Might Contribute to Chronic Stress-Induced Atrophy of Hippocampal Astrocyte volume and Depression-like Behavior in Rats

Inducible nitric oxide synthase is involved in the modulation of depressive behaviors induced by unpredictable chronic mild stress

Inhibition of iNOS alleviates cognitive deficits and depression in diabetic mice through downregulating the NO/sGC/cGMP/PKG signal pathway.

Health-related Quality of Life, Depression and Anxiety in Thyroid Cancer Patients

Brain Iron Overload, Insulin Resistance, and Cognitive Performance in Obese Subjects: A Preliminary MRI Case-Control Study

High intelligence: A risk factor for psychological and physiological overexcitabilities

Mitochondrial function in the brain links anxiety with social subordination

Assessment of Anxiety in Subclinical Thyroid Disorders

Glial Cell Glycogen and Stress-induced Depression

A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle.

Depression, anxiety, and somatization in patients with clinical and subclinical hypothyroidism: An exploratory study

Socially responsive effects of brain oxidative metabolism on aggression

Effects of neurosteroids on the human corticotropin-releasing hormone gene.

Higher Body Iron Is Associated with Greater Depression Symptoms among Young Adult Men but not Women: Observational Data from the Daily Life Study

A meta-analysis of lipid peroxidation markers in major depression

Prevalence of anxiety and depressive symptoms among patients with hypothyroidism

Brain glycogen re-awakened

Improvement of mitochondrial energy and oxidative balance during intestinal differentiation.

Neurometabolic Disorders: Potentially Treatable Abnormalities in Patients With Treatment-Refractory Depression and Suicidal Behavior

Oral administration of inosine produces antidepressant-like effects in mice

Brain glycogen—new perspectives on its metabolic function and regulation at the subcellular level

Frontal Dysfunction Underlies Depression in Mild Cognitive Impairment: A FDG-PET Study



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