High Anxiety, When Sugar Falls.

sugaaa I’m going to talk about anxiety. Not so much the external factors that help to create or worsen it: environmental stress; chronically difficult social interactions and relationships; hereditary predispositions; early life and present day trauma.

“Notably, within the SAD (Social Anxiety Disorder) group, the rate of serotonin synthesis in the dorsal amygdala correlated positively with severity of social anxiety symptoms…results suggest that increased extracellular serotonin concentration underlies elevated anxiety and amygdala responsivity in SAD.”

This won’t be a discussion focusing on the pharmaceutical products – a small number of which can be very helpful – or of the many other methods used to try and manage what can potentially become an ongoing and debilitating issue.

“…most frequently Sexual Difficulties (62%) and Feeling Emotionally Numb (60%). Percentages for other effects included: Feeling Not Like Myself – 52%, Reduction In Positive Feelings – 42%, Caring Less About Others – 39%, Suicidality – 39% and Withdrawal Effects – 55%…adverse effects of antidepressants may be more frequent than previously reported…”

“…results of the study showed that cyproheptadine is effective in prevention of depression, anxiety, hallucination, aggressive behaviors, emotional withdrawal, poor rapport, poor impulse control, active social avoidance, suicidal ideation, and improved sleep quality…”

It will also not be an attempt to give a step by step prescription as to how to eradicate anxiety in just 3 simple steps.

What I want to talk about mostly, is how the degree of anxiety experienced by a person, isn’t always dependent upon the objectively stressful nature of their particular life circumstances.

Why is it that anxiety can be something which seems to come and go for no apparent reason – or be there constantly in the background – regardless of how relatively stress-free a persons life appears to be?

“Clinical theories posit interpersonal stress as an important factor in…anxiety, while neuroendocrine research confirms the association…with dysregulation in a major stress response system, the hypothalamic-pituitary-adrenal (HPA) axis.”

“…anxiety sensitivity (AS)…interacts with ovarian hormonal changes that occur during the premenstrual phase of the menstrual cycle, which affects behavioral and physiological responses to stress, subsequently initiating or maintaining clinical panic and/or anxiety.”

“…experimental research indicates that 5HT (serotonin) can act directly on the adrenal gland and possibly on the anterior pituitary as well. These findings have major implications for the interpretation of neuroendocrine studies of 5HT conducted in psychiatric conditions…”

Susceptibility to chronic anxiety is probably always going to be related to some kind of interaction with environmental factors, and this can include traumatic early life experiences and all kinds of other stress promoting things.

It is a perfectly valid and useful approach to consider the external influences which might be driving anxiety, and attempt to remove or improve them.

But it is also true to say that feelings of anxiety cannot really be understood independently of the particular physiological state or condition of the individual. Sometimes it is these biological factors which can more easily be tweaked in order to help create a buffer against stress and eventually reduce symptoms.

“…data reveal a discrete 5-HT (serotonin) responsive circuit…that underlies pathological anxiety and fear associated with a hyperserotonergic state…SSRIs are currently a first-line treatment for anxiety and panic disorders, but can acutely exacerbate symptoms…”

“Our work identifies trait anxiety as a predisposing factor to a subordinate rank. We demonstrate that mitochondrial function…is a critical mediating factor…Limited energy production…may impair adaptive neuronal capacity to life challenges and contribute to the development of psychopathologies…”

Although it isn’t a popular viewpoint, there is plenty of experimentation looking at the impact of stress upon metabolic function, and how that can eventually create the kind of energy preserving inhibitory harm avoidance/learned helplessness state which involves anxiety and social phobia.

“..the increase in whole brain serotonin turnover in patients with panic disorder “most likely derived not from impaired serotonin reuptake, but from increased firing in serotonergic midbrain raphe neurons projecting to both subcortical brain regions and the cerebral cortex” Indeed, many researchers consider anxiety to be a state of elevated serotonin transmission…”

The substances which rise under stress – including cortisol, adrenalin, serotonin and estrogen – powerfully interact with each other in ways that help to suppress thyroid energy metabolism, interfering with production of the protective hormones (pregnenolone, progesterone and others), impacting upon brain function.

“Estrogen receptors are widely distributed in the brain, including the limbic system and the hypothalamus…Our findings implicate…the HPA axis, as a potentially important target of ovarian steroids and a potential mediator of gender related differences in the stress response and HPA axis activity…”

The more stress one is exposed to – especially early in life – the higher the likelihood that a metabolically suppressed state will become self-perpetuating, creating conditions enabling the stress system to be more easily activated.

It can get to a point where it is difficult to avoid triggering an anxiety response, regardless of how stressful circumstances are – ‘objectively’ speaking – making it appear sometimes as if the response is unrelated to external conditions.

A big reason behind the circular nature of anxiety, is because the biochemical factors which have been shown to promote the anxiety response – serotonin, cortisol and estrogen for instance – can also impact upon perception, increasing the sense of fear or imminent danger in any scenario. This can then worsen the biologically stressful nature of conditions and on and on.

“Children with antisocial and aggressive behaviors have been found to show abnormal neurobiological responses to stress, specifically impaired cortisol stress reactivity…those with comorbid anxiety showed impaired cortisol recovery, whereas those without anxiety showed reduced baseline cortisol levels.”

“Considerable investigation has…been directed toward identifying the neurobiological mechanisms whereby psychosocial risk factors enhance the activity of the HPA axis. There is now a growing consensus that serotonin acts at multiple sites to contribute to stress-induced HPA axis activation…”

“Pretreatment…with…THP (allopregnanolone) significantly attenuated the elevation of plasma adrenocorticotropin (ACTH) and serum corticosterone after emotional stress…”

This kind of vicious circle does not only occur in relation to social hardship, but rather can exist as a result of anything physiologically stressful. Even though there can be enormous variation from one person to the next in terms of resilience to stress, the same biological principles apply across the board.

Some things are protective and other things are likely to cause harm. But sensitivity varies as a result of a multitude of influencing factors.

Fear or anxiety uses up glycogen stores, and when levels run low, cortisol and adrenalin rise as a means to providing needed fuel. This process involves the release of fat out of storage and the breakdown of muscle, glands and other tissue, which can promote stress and inflammation, and thus more potential for anxiety.

“Dysregulation of the stress axis…characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety…available data suggest that targeting inflammation may serve as a potential therapeutic target…”

Greater amounts of circulating polyunsaturated fats (PUFA) easily fuel a chronic inflammatory state, and the breakdown products of PUFA have been demonstrated to be involved in many conditions where chronic anxiety is a symptom.

“…latest findings show that the pathophysiology of anxiety disorders might be associated with oxidative stress and lipid peroxidation…Serum levels of lipid hydroperoxide (LOOH) are a reliable marker of lipid peroxidation…LOOH levels were significantly higher in the anxiety disorders group than in the control group…”

“Our study reveals that GAD (Generalized Anxiety Disorder) patients have considerably higher level of malondialdehyde (breakdown product of PUFA), immunoglobulins and altered level of antioxidant vitamins…”

PUFA also directly interferes with blood sugar regulation and thyroid function, leading to a rise in levels of bacterial toxins (such as endotoxin) throughout the system. Endotoxin exposure leads to more of the inflammatory things – including cortisol, serotonin, estrogen, nitric oxide and PUFA – all of which have been shown to feed anxiety.

“LPS [endotoxin] administration in healthy male subjects induced a transient, dose-dependent inflammatory response characterized by increases in body temperature and heart-rate, plasma concentrations of pro- and anti-inflammatory cytokines, cortisol, and norepinephrine. In parallel, we observed dose-dependent increases in negative mood and anxiety.”

“…glutamate and nitric oxide (NO) play a causal role in anxiety-related behaviors…Acute stress is…associated with the release of glucocorticoids, as well as 5HT, glutamate, and NO in the hippocampus.”

Harmful effects of what is referred to as PTSD are known to be connected to increased cortisol levels in response to chronic and acute stress, and lack of sugar availability or accessibility encourages cortisol and PUFA release (and inhibits production of the protective hormones like testosterone), promoting a self-feeding stress state which can damage the brain.

“PTSD is generally regarded as a disorder of dysregulated threat reactivity. In line with this view, the peritraumatic period is marked by elevated cortisol and stress-evoked cortisol hyper-reactivity…testosterone’s anti-glucocorticoid effects may protect against structural damage in the hippocampus…producing long-term protection against the stress-evoked glucocorticoid-mediated neural degeneration thought to characterize PTSD…”

Hyperventilation (or over-breathing) is a common response to fear or anxiety. Hyperventilation lowers carbon dioxide (CO2) levels, increasing overall susceptibility to stress, and promoting many of the inflammatory anxiety producing things including serotonin. Serotonin can then cause further hyperventilation.

“Given habitual hyperventilation, a variety of triggers…can initiate the vicious cycle of increased breathing, symptoms, anxiety arising from symptoms exacerbating hyperventilation and thus generating more symptoms and more anxiety.”

“Intravenous administration of 5-hydroxytryptamine (Serotonin) caused a large increase in ventilatory frequency…and amplitude…The 5-hydroxytryptamine-induced hyperventilation was blocked by the 5-HT3-receptor antagonists…”

With this in mind, it’s easy to see why sugar restriction is probably one of the worst dietary strategies for dealing with chronic anxiety.

Sugar is necessary to maintain thyroid function, and thyroid function protects against the loss of carbon dioxide due to hyperventilation. Sugar and good thyroid activity is also necessary for the production of enough of the brain protective hormones – progesterone and pregnenolone – which also protect against the loss of CO2 and a chronic anxiety state.

“…serum concentrations of pregnenolone have been shown to be lowered in patients with generalized anxiety disorder and with generalized social phobia…”

“…evidence suggests that stress-induced increases in progesterone and allopregnanolone may be an endogenous mechanism that counteracts increases in anxiety and limits hypothalamic pituitary adrenal axis activation.”

Simple white sugar can be used as part of a therapeutic strategy attempting to reverse – or minimise – the processes at play behind anxiety conditions. These processes make it difficult to return to a thyroid driven metabolism, and in the absence of enough fuel and other nutrients it can be difficult to turn down nervous system over-stimulation.

“…the metabolically restorative effects of sucrose may, in part, mediate sucrose-induced inhibition of central stress reactivity…ingestion of sucrose…reduced stress-induced increases in circulating cortisol.”

It’s not a black and white scenario, and it isn’t always enough to just increase your intake of white sugar for all to be rosy.

There are lots of possible variations to diet and lifestyle that can be experimented with in order to see significant and lasting results.

They should all be part of an attempt to redirect away from a stress metabolism – and towards improvements in energy system performance – and the inclusion of sufficient sugar consumption can play a significant role.

Increased intake of sugar – in combination with enough easily digested protein and nutrients (including sodium, magnesium and calcium) – to assist in settling down the stressed, over-excited nervous system and to lower inflammation, can improve resilience against chronic anxiety conditions, becoming increasingly common regardless of life circumstances.

Some other things that have been shown to help protect against anxiety include coffee, aspirin, certain antihistamines, minocycline, regular bag breathing, theanine, magnesium, salt, methylene blue, pregnenolone, progesterone, glycine, niacinamide, thyroid hormone as well as taurine.

These kinds of approaches are sometimes enough to create the opening required to let in a whole range of lifestyle changes, which can eventually reduce or protect against anxiety, and change a persons whole outlook and life.

See More Here

Serotonin Synthesis and Reuptake in Social Anxiety Disorder

Serotonin States and Social Anxiety

Prevention of stress-induced morphological and cognitive consequences.

Traumatic stress: effects on the brain

Hyperventilation in Panic Disorder and Asthma: Empirical Evidence and Clinical Strategies

Psychoregulating role of nicotinamide.

Behavioral, neurochemical and endocrinological characterization of the early social isolation syndrome.

Mitochondrial function in the brain links anxiety with social subordination

Dual-hormone stress reactivity predicts downstream war-zone stress-evoked PTSD.

Effect of dietary salt restriction on urinary serotonin and 5-hydroxyindoleacetic acid excretion in man.

Norepinephrine stimulates testosterone aromatization and inhibits 5 alpha reduction via beta-adrenoceptors in rat pineal gland.

Rapid recovery from major depression using magnesium treatment.

Sex differences in corticotropin-releasing factor receptor signaling and trafficking: potential role in female vulnerability to stress-related psychopathology

Protective effect of l-theanine on chronic restraint stress-induced cognitive impairments in mice.

Serotonin reuptake inhibitors act centrally to cause bone loss in mice by counteracting a local antiresorptive effect

Testosterone rapidly reduces anxiety in male house mice (Mus musculus).

Increased aerobic glycolysis through beta2 stimulation is a common mechanism involved in lactate formation during shock states.

Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Dose-related anxiogenic effect of glycine in the elevated plus maze and in electrodermal activity.

Is aspirin, as used for antithrombosis, an emotion-modulating agent?

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

Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents: a network meta-analysis.

Effects of aspirin on immobile behavior and endocrine and immune changes in the forced swimming test: comparison to fluoxetine and imipramine.

Acute stress persistently enhances estrogen levels in the female rat.

Benzodiazepine use and risk of Alzheimer’s disease: case-control study

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

Recurrent Hypoglycemia Increases Anxiety and Amygdala Norepinephrine Release During Subsequent Hypoglycemia.

Anxiety-like behavior in the elevated-plus maze tests and enhanced IL-1β, IL-6, NADPH oxidase-1, and iNOS mRNAs in the hippocampus during early stage of adjuvant arthritis in rats.

Adverse emotional and interpersonal effects reported by 1829 New Zealanders while taking antidepressants

Hyperventilation and anxiety state

Developmental minocycline treatment reverses the effects of neonatal immune activation on anxiety- and depression-like behaviors, hippocampal inflammation, and HPA axis activity in adult mice.

Psychoregulating role of nicotinamide.

Co-occurrence of anxiety and depressive-like behaviors following adolescent social isolation in male mice; possible role of nitrergic system.

Do non-steroidal anti-inflammatory drugs influence the steroid hormone milieu in male athletes?

Dose-Dependent Effects of Endotoxin on Neurobehavioral Functions in Humans

The effects of caffeine and aspirin on mood and performance.

Serotonin and the regulation of hypothalamic-pituitary-adrenal axis function.

Anxiety Sensitivity, the Menstrual Cycle, and Panic Disorder: A Putative Neuroendocrine and Psychological Interaction

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

Asthma and depressive and anxiety disorders among young persons in the community.

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

Endotoxin exposure in early life alters the development of anxiety-like behaviour in the Fischer 344 rat.

Anxiety after cardiac arrest/cardiopulmonary resuscitation: exacerbated by stress and prevented by minocycline.

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond.

Insulin resistance in brain alters dopamine turnover and causes behavioral disorders

Nitric oxide as inflammatory mediator in post-traumatic stress disorder (PTSD): evidence from an animal model

Serotonin activates the hypothalamic-pituitary-adrenal axis via serotonin 2C receptor stimulation.

Comparative analysis of serum malondialdehyde, antioxidant vitamins and immunoglobulin levels in patients suffering from generalized anxiety disorder.

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

Anxiolytic and antidepressant properties of methylene blue in animal models.

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

Mediation of serotonin-induced hyperventilation via 5-HT3-receptor in European eel Anguilla anguilla.

Methylene blue treatment for residual symptoms of bipolar disorder: randomised crossover study.

Oxidative Imbalance and Anxiety Disorders

Cyproheptadine for combat nightmares in post-traumatic stress disorder and dream anxiety disorder.

Cortisol responses to emotional stress in men: Association with a functional polymorphism in the 5HTR2C Gene

Anxiety disorders and GABA neurotransmission: a disturbance of modulation

Association Between Mental Disorders and Physical Diseases in Adolescents From a Nationally Representative Cohort

Protective effect of l-theanine on chronic restraint stress-induced cognitive impairments in mice.

The neurosteroid tetrahydroprogesterone attenuates the endocrine response to stress and exerts glucocorticoid-like effects on vasopressin gene transcription in the rat hypothalamus.

Taurine induces anti-anxiety by activating strychnine-sensitive glycine receptor in vivo.

Physiological and behavioral responses to corticotropin-releasing factor administration: is CRF a mediator of anxiety or stress responses?

The relationship between adverse events during selective serotonin reuptake inhibitor treatment for major depressive disorder and nonremission in the suicide assessment methodology study.

Depression and anxiety predict sex-specific cortisol responses to interpersonal stress.

Cyproheptadine for prevention of neuropsychiatric adverse effects of efavirenz: a randomized clinical trial.

[Study of the stress response: role of anxiety, cortisol and DHEAs].

Anxiety levels parallel changes in inflammation over time in ovarian cancer patients

End-tidal CO2 levels lower in subclinical and overt hypothyroidism than healthy controls; no relationship to thyroid function tests

Efficacy of cyproheptadine for nightmares associated with posttraumatic stress disorder.

Parental history of depression or anxiety and the cortisol awakening response.

Allopregnanolone modulation of HPA axis function in the adult rat.

The evaluation of anxiety and salivary cortisol levels in patients with oral lichen planus.

The role of anxiety in cortisol stress response and cortisol recovery in boys with oppositional defiant disorder/conduct disorder.

Lactate-mediated glia-neuronal signalling in the mammalian brain


Image: Sugar vaincue

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