What is Melatonin?

Melatonin is derived from the amino acid tryptophan and the neurotransmitter serotonin [R].

Melatonin has many important functions in the body, including:

• Influences the circadian rhythm
• Aids the immune system
• Helps eye function
• Reduces oxidative stress
• Promotes sleep
• Controls many cellular events, including synthesis of important molecules
• Protects against radiation

The pineal gland, which is nestled in the brain, makes melatonin. The quantity of melatonin in the blood depends on the time of the day. At night there is 10 to 15 times more melatonin in the blood there is in the day, which helps people sleep [R].

Melatonin is also made by many other organs in the body, especially in the stomach [R].

If sleep is interrupted by blue light exposure at night, melatonin levels decrease drastically. In addition, melatonin levels also decrease with age [R]. However, darkness does not stimulate melatonin production. It simply permits melatonin production [R].

Potential Benefits of Melatonin

Melatonin supplements have not been approved by the FDA for medical use. Supplements generally lack solid clinical research. Regulations set manufacturing standards for them but don’t guarantee that they’re safe or effective. Speak with your doctor before supplementing.

Possibly Effective For

1) Endometriosis

Surprisingly, melatonin has shown promise for reducing pain in endometriosis. In a study of 40 women of reproductive age, 10 mg of melatonin per day reduced pain scores and dysmenorrhea by almost 40% each. Women who took melatonin also used fewer painkillers [R].

2) Blood Pressure

Melatonin plays an important role in the regulation of blood pressure. Activation of its receptors, MT1 and MT2, widens blood vessels, which decreases blood pressure [R].

Like sleep, blood pressure has circadian rhythmicity. It increases in the morning and decreases at night. Melatonin rises at night and decreases in the morning. This indicates that there may be a connection between melatonin and blood pressure [R].

Certain types of hypertension (high blood pressure) are characterized by low melatonin [R].

In patients with type 2 diabetes, 5 mg of melatonin decreased blood pressure levels. However, there is not enough information about how melatonin reduces blood

The post 9+ Benefits of Melatonin for Anxiety, Depression, Gut & More appeared first on SelfHacked.

Genes play an important role in this condition. If you have a sibling with Hashimoto’s, you have twice the risk of developing the disease. If one of your parents has Hashimoto’s, then you may have triple the risk of developing the disease [R].

Genes That May be Involved in Hashimoto’s

It’s important to note that just because certain genotypes are associated with a condition or irregular lab marker, it doesn’t necessarily mean that everyone with that genotype will actually develop the condition. Many different factors, including other genetic and environmental factors, can influence the risk of Hashimoto’s disease.

1) ZFAT (Cell Survival Gene)

ZFAT codes for a protein that has a specialized structure to help it recognize DNA important to cell development and immunity [R, R, R].

Reduced production of ZFAT has been associated with cell death in connective tissue and problems with cell development [R].

Having a T variant for Ex9b-SNP10 at intron 9 is associated with increased rates of autoimmune thyroiditis [R].

2) PTPN22

PTPN22 encodes a protein that prevents the activation of immune cells called T-cells (involved in H inhibitor of T-cell activation. The SNP rs2476601 is associated with Hashimoto’s in some populations, but not others [R, R].

3) Tg

The Thyroglobulin (Tg) gene is involved in the synthesis of thyroid hormones T4 and T3. SNPs of the Tg gene at exon-33 may predispose people to autoimmune thyroid diseases, although the exact mechanisms are unknown. The D8S272 marker is indirectly linked to susceptibility to autoimmune thyroid diseases [R].

The 1623 A/G SNP of the Tg gene promoter (rs180195) is associated with Hashimoto’s thyroiditis. Individuals with Hashimoto’s are more likely to have the A allele [R].

4) VDR

The Vitamin D receptor gene (the “sunshine gene”) is critical for Vitamin D absorption. Mutations in the vitamin D receptor gene can cause vitamin D deficiency (<30 ng/mL) [R].

Vitamin D deficiency is positively correlated with increased thyroid antibodies, a common feature of autoimmune thyroid diseases [R].

5) HLA-B

HLA-B gene mutations may correlate with Hashimoto’s thyroiditis among Han Chinese people, according to a study of 488 participants [R].

The post Hashimoto’s Thyroiditis Genetic Factors appeared first on SelfHacked.

Prevalence and Epidemiology

Multiple sclerosis (MS) was first described, illustrated, and documented in 1838 by Sir Robert Carswell, a Scottish Professor of Pathology, but it was not officially named until 1955 [R, R].

The popular epidemiological notion is that MS frequency increases with geographic latitudes [R].

We still don’t fully understand why MS is more prevalent in these regions, but a growing body of evidence indicates a role of inadequate sun exposure and vitamin D levels [R, R].

According to the Atlas: Multiple Sclerosis Resources in the World 2008 published by the World Health Organization (WHO), the global median estimated prevalence for multiple sclerosis is 30 per 100,000 individuals [R].

The incidence of multiple sclerosis is low in childhood but drastically increases after 18 years of age, peaking around 25 to 35 years and declining after [R].

In 2015, about 18,500 individuals died from multiple sclerosis [R].

Despite these numbers, multiple sclerosis only marginally reduces the life expectancy of an individual but greatly diminishes the quality of life [R].

Multiple Sclerosis Genes

It’s important to note that just because certain genotypes are associated with a condition or irregular lab marker, it doesn’t necessarily mean that everyone with that genotype will actually develop the condition. Many different factors, including other genetic and environmental factors, can influence the risk of multiple sclerosis.

Different ethnic populations around the world have different prevalence and susceptibility to multiple sclerosis that cannot be explained by environmental factors alone [R].

Individuals with relatives affected by multiple sclerosis have a higher probability of developing the disease [R].

Identical twins have a 30% chance of both developing MS if one of them develops it. First-degree relatives of individuals affected by multiple sclerosis are 10 – 25 times more likely to develop the disease than the general population [R, R].

Genetic variations may play a role in multiple sclerosis. Several genetic regions have been implicated in the development of the disease. The most prevailing genes are the HLA genes which are contained in the major

The post Multiple Sclerosis Genes, Epidemiology & Prevention appeared first on SelfHacked.

What is Multiple Sclerosis?

Multiple sclerosis (MS) is a chronic autoimmune debilitating disease in which nerve damage (demyelination of neurons) in the brain and spinal cord disrupts their communication with the body.

MS is a leading cause of disability in young adults and is the most common inflammatory disorder of the brain. It’s most common in young women, but other groups can be affected, too [R].

.

Diagnosis and Symptoms of MS

Demyelination and damage to neuronal axons can lead to many observable negative health effects and symptoms associated with multiple sclerosis. Clinical diagnosis can be made through medical imaging (MRI) and laboratory testing (CSF testing) [R].

While MS symptoms vary greatly from patient to patient, these commonly include [R, R, R, R, R]:

• Painful eye movement and blurred vision (damage to the optic nerve)
• Tremors and loss of coordination/balance (damage to the cerebellum)
• Limb and muscle weakness, spasms, and numbness lead to mobility problems (damage to the spinal cord)
• Electric-shock sensations provoked by neck movements (Lhermitte sign)
• Blurred or double vision (damage to the brainstem)
• Constipation, incontinence, bladder problems, or erectile dysfunction (loss of upper motor neuron control)
• Speech impairment and trouble swallowing; however, only a small percent of MS patients are affected by these symptoms (impairment of motor speech processes in the brainstem)
• Memory and cognitive problems
• Fatigue, which may potentially coexist with depression
• Depression: MS is strongly correlated with depression – up to 41.8% of MS patients has clinical depressive symptoms

Given that MS patients display different symptoms unique to themselves, the management should be tailored to the patient and each symptom mitigated individually. Patients facing fatigue and muscle weakness can undergo physical therapy to be able to undertake daily activities [R].

Based solely on these symptoms, MS is difficult to diagnose non-invasively because the disease shares many symptoms with other neurological disorders such as acute disseminated encephalomyelitis and neuromyelitis optica. As a result,

The post Multiple Sclerosis (MS): Causes, Symptoms & Diagnosis appeared first on SelfHacked.

When discussing issues with the BBB, it is important to note that a problem does not always start in the brain. Diseases and other problems elsewhere in the body, such as diabetes or gut inflammation, may trigger a “leaky brain.” In this post, we cover the top 11 factors that can disrupt the blood-brain barrier.

Brain Injuries

1) Stroke

Strokes cause a lack of glucose and oxygen. This leads to a rise in potassium, the depletion of ATP, and a release of glutamate, which all contribute to blood-brain barrier disruption [R].

Under stroke conditions, the tight junctions that help prevent substances from entering the brain have compromised integrity. This means that the tight junctions are weaker and increase BBB permeability [R].

After a stroke, reperfusion (restoration of blood flow to the brain or tissue) occurs. Reperfusion may cause additional tissue damage and an increase in inflammation, which also worsens the BBB condition [R].

In a study of human brain tissue from five cases of fatal strokes, MMP9 levels were higher in the affected areas. Higher MMP9 levels are a good indicator of increased BBB permeability [R].

2) Traumatic Brain Injury

https://www.ncbi.nlm.nih.gov/pubmed/25624154

After traumatic brain injury, the blood-brain barrier also becomes dysfunctional. This leads to the leakage of proteins and negatively affects immune cells [R].

BBB breakdown may last from several days to weeks after head trauma. In some cases, the BBB can be dysfunctional for years [R].

Head trauma injures blood vessels in the brain. It leads to impairments in brain-blood flow, BBB permeability, and metabolic processes. It also reduces oxygen levels in the brain, which further induces BBB breakdown [R].

Traumatic brain injuries also cause damage to the neurovascular unit. When the nerve cells die quickly, it causes another cycle of injury after the initial brain injury [R].

After traumatic brain injury, excessive superoxide reacts with nitric oxide to form peroxynitrite. Peroxynitrite contributes to BBB leakage [R].

In traumatic brain injury-induced adult male rats, treatment to reduce peroxynitrite also decreased BBB leakage. S-nitroso-glutathione (GSNO) helps stop BBB dysfunction and provides protection to nerve

The post 11 Factors That Disrupt the Blood-Brain Barrier appeared first on SelfHacked.

Sleep and Neurotransmitters

The neural control of sleep is like a seesaw between the sleep and wakefulness state, which is controlled by orexin neurons.

During sleep, neurons in the hypothalamus produce sleep neurotransmitters such as GABA and galanin and inhibit dopamine, histamine, norepinephrine and serotonin neurons (monoaminergic neurons).

During wakefulness, neurons secrete dopamine, histamine, norepinephrine, and epinephrine while inhibiting GABA.

1) Orexin/Hypocretin

Orexin, also called hypocretin, is a neuropeptide that increases arousal, wakefulness, and appetite. Orexin-producing neurons work during active wakefulness and stop during sleep (R).

The importance of orexin in the maintenance of sleep/wake cycle was first demonstrated by the fact that orexin deficiency caused narcolepsy in humans and animals (R, R, R, R).

A lack of orexins correlates with narcolepsy. Approximately 90% of patients with narcolepsy (with cataplexy) show decreased orexin-A levels in the cerebrospinal fluid (CSF, the fluid surrounding the brain) (R).

Mice lacking the gene for orexin showed phenotypes similar to humans with narcolepsy and disruption of the hypocretin receptor 2 (Hcrtr2) caused canine narcolepsy (R, R, R).

Both noradrenaline and serotonin can inhibit the activity of orexin neurons (R, R).

Loss of function in the orexin neurons is also involved in altered energy homeostasis, which could result in fatigue (R).

Read this post to learn more about the orexin system and ways to ensure it functions well.

2) Dopamine

Dopamine functions as a neurotransmitter and is crucial for arousal, memory and motor function (R).

Altered brain dopamine leads to several neurological disorders like Parkinson’s, schizophrenia and ADHD (R, R).

Individuals with these diseases show dramatic sleep disturbances, including excessive daytime sleepiness, rapid-eye sleep movement disorder, decreased REM sleep and disturbed sleep architecture (R, R).

These observations show that dopamine function and dopamine receptors may play a role in regulating sleep-wake cycles. Generally, high dopamine induces wakefulness while blocking dopamine receptors promotes sleep.

Activation of the D1 dopamine receptor increases wakefulness and reduces slow-wave sleep and REM sleep (

The post How Brain Health & Neurotransmitters Affect Sleep appeared first on SelfHacked.

Disclaimer: This post is not a recommendation for any particular type of MS treatment. Make sure to discuss your options with your personal doctor; none of the complementary approaches described below should be used to replace medical treatment. The goal of this post is simply to inform our readers about the science and evidence behind some potential complementary approaches to MS, which may or may not be effective.

Conventional MS Treatment

Although there is no universal cure for MS, several therapies have proven effective in preventing the progression and relapses of the disease. There are no known therapies that promote the regeneration of these deficits because MS damages neurons in the brain [R].

Spontaneous recovery is rare if the damage to the neurons has progressed longer than 6 months [R].

MS’s long-term disability progresses slowly over many years. As a result, many treatments mitigate the short-term symptoms of the disease [R].

1) Glucocorticoids

A patient with MS (relapsing-remitting MS or primary progressive MS) will commonly face relapses or attacks, which are flare-ups of new or recurring symptoms. Administration of high doses of glucocorticoids (methylprednisolone) or corticosteroids is the current routine therapy for acute relapses [R, R].

The advantages of using glucocorticoids include rapid functional recovery in patients with acute attacks [R].

Limitations

Administration of intravenous glucocorticoid can lead to potential side effects such as reddening of the face, ankle swelling, and a metallic taste in the mouth. Oral administration of glucocorticoids has more side effects including disturbed sleep, mood changes, and stomach problems [R].

Also, glucocorticoids only mitigate the short-term symptoms of MS without dealing with the long-term effects [R, R].

High doses of glucocorticoids will not affect long-term disease improvement because of the treatment’s limited effects on MS lesions in the brain. The irreversible damages are not being regenerated [R].

Glucocorticoids may also have detrimental effects on bone density, increasing the risk of bone fracture [R].

2) Disease-Modifying Therapies

Disease-modifying therapies (DMTs) were created

The post Multiple Sclerosis (MS): Diets & Complementary Approaches appeared first on SelfHacked.

What is Stevia?

Stevia was originally called Eupatorium rebaudiana bertoni in honor of Rebaudi, who was the first chemist to study the chemical characteristics of the plant’s extracts (R).

It was first used as a sweetener in herbal fusions by the Guarani people of South America, but Japan was the first country to market steviol glycosides in the food and drug industry.

Now, cultivation of the plant has expanded to other Asian regions like China, Malaysia, Singapore, South Korea, Taiwan, and Thailand. The plant is a long-lasting shrub that is over 100 to 300 times sweeter than table sugar and has no calories [R, R].

Traditional Uses

Indigenous people of South America, particularly in Paraguay and Brazil, have used stevia as a sweetener for hundreds of years. For example, the Gurani Indians of Paraguay have an age-old practice of using stevia to sweeten their Yerba Mate tea.

South American populations also have a long history of using stevia medicinally, as a tonic for heart problems, obesity, high blood pressure, and heartburn.

Stevia was first noticed by the outside world in the sixteenth century when Spaniards discovered the widespread use of stevia in South America.

In recent years, a growing need to find new, naturally sweet, calorie-free alternatives to sugar has led to greater interest in the “sweet herb” from nutritional researchers and commerce (R).

Constituents

The best known natural products derived from stevia rebaudiana are glycosides such as stevioside (9.1%), rebaudioside A (3.8%), rebaudioside C (0.6%), steviolbioside (a.k.a. steviol), dihydroisosteviol (a.k.a. isosteviol), rubusoside, and dulcoside (0.3%).

Stevia consists of approximately 80 – 85% percent water, protein, fiber, fats, monosaccharides, essential oils, vitamin c, β-carotene, vitamin B2, and vitamin B1.

It also contains minerals like cobalt, magnesium, iron, potassium, and phosphorus. Certain antioxidant compounds are also elements in stevia.

Health Benefits of Stevia

Possibly Effective:

1) High Blood Pressure

In a meta-analysis of nine studies and 756 participants, steviol glycosides caused a considerable decrease in diastolic (lower) but not systolic (higher) blood pressure. The results were most effective when observed over a long period of time (R

The post Health Benefits of Stevia + Dosage & Safety appeared first on SelfHacked.

What Are Short Chain Fatty Acids (SCFA)?

Short-chain fatty acids (SCFAs; acetic, propionic and butyric acid) are formed during bacterial fermentation of carbohydrates in the colon.

SCFAs cause low intestinal pH from the ileum (end of the small intestine) to the cecum (beginning of large intestine), which prevents the overgrowth of bad bacteria (like Enterobacteriaceae and Clostridia) (R).

SCFAs help fix ‘leaky gut’, strengthening the intestinal wall by increasing the secretion of mucin-2 (MUC-2), which then prevents LPS from crossing the barrier (R).

SCFAs In the Human Gut

Out of the total SCFAs present in the colon, 90%-95% are acetate, propionate, and butyrate in healthy people.

• Acetate 60%
• Propionate 25%
• Butyrate 15%

Most of the SCFAs are absorbed in the colon, being exchanged with bicarbonate (R).

SCFAs are acidic, while bicarbonate is alkaline.

SCFAs and Obesity

There is some conflicting information on SCFAs and weight. On the one hand, they increase caloric utilization. On the other hand, they have been inversely associated with obesity. Overall, butyrate seems to be broadly protective against obesity, propionate has mixed associations, and acetate is linked to weight gain (R).

The fecal concentration of SCFAs is 20% higher in obese individuals than in their lean counterparts. According to some researchers, this may reflect a compensatory protective mechanism against obesity, in which a greater amount is eliminated from the stool (R).

This would prevent the increased accumulation of SCFA in the intestines, which may cause weight gain (mainly from acetate) (R).

SCFAs like butyrate and propionate increase the formation of the gut hormones glucagon-like peptide-1 (GLP-1) and polypeptide YY (PYY). These reduce food intake by decreasing appetite (R).

Butyrate

Butyrate reduces food intake and has been linked to weight loss.

Researchers are also investigating butyrate’s potential to combat autoimmunity, cancer, and psychological disorders. Butyrate, which is primarily produced by Firmicutes bacteria in the gut, appears to affect gene expression in the brain (R, R).

Butyrate is primarily used by colon cells as a major source of energy

The post How Your Gut Microbiota Can Make You Fat (or Thin) appeared first on SelfHacked.

Synaptic Plasticity: A Quick Review

Synaptic plasticity refers to the brain’s ability to adjust how neurons connect to and “talk” to each other, which in turn affects how the brain processes information.

Synaptic plasticity is critical to our ability to learn and store new knowledge and memories, since the brain has to be able to change its structure in order to encode new information and facts!

Deficits and other changes in the cellular processes underlying synaptic plasticity are also believed to be involved in a wide range of neurological and psychiatric disorders, making it very important for overall brain health and psychological well-being.

P.S: For a more detailed overview of what synaptic plasticity is, how it works, and why it’s important, check out our detailed SelfDecode post all about synaptic plasticity here.

Dietary Compounds And Supplements That May Increase Synaptic Plasticity:

According to some preliminary research, there may be a number of foods and dietary compounds that may support or stimulate synaptic plasticity throughout the brain [R, R].

However, whether consuming the foods and supplements below can actually result in noticeable changes in cognitive function is still an open question. While there is some early research with promising results so far, a lot more research will be needed to fully confirm these effects in healthy human users, and so far there is “insufficient evidence” to officially recommend these strategies for enhancing cognitive functions or treating diseases. Therefore, these early findings should be taken with a grain of salt until more extensive research is done to figure out their full effects.

With that in mind, let’s see what some of the latest science has to say about some nutritional compounds and dietary supplements that may potentially help boost synaptic plasticity!

INSUFFICIENT EVIDENCE:

1) Polyphenols May Stimulate Synaptic Plasticity

Fruits, vegetables, cereals, and beverages contain natural polyphenols. Grapes, apples, pears, cherries, and berries may contain up to 200-300 mg of polyphenols in each 100-gram serving [R].

Phenolic acids, flavonoids, phenolic amides, resveratrol, lignans, curcumin, rosmarinic

The post 19 Potential Ways to Stimulate Synaptic Plasticity appeared first on SelfHacked.

What is Synaptic Plasticity?

It was once believed that the brain is extremely fragile, and that any damage to it is more or less permanent. This would mean that if a person’s brain was damaged or failed to develop properly in the first place, they were fated to live with it permanently!

However, the discovery of synaptic plasticity in 1966 overturned that belief. This gave new hope to people with brain damage, neurological diseases, or learning disabilities [R].

In fact, the brain is a lot more flexible and resilient than we previously thought! Neurons can re-grow and new neuronal connections can be made. This actually allows us to learn new skills and memories in everyday life since the brain is a physical organ, and therefore, has to change its structure in order to store any new information.

Synaptic plasticity is our brain’s key to the formation of new memories and neural networks – especially within the hippocampus, a brain structure that is believed to be heavily involved in memory.

Furthermore, neural plasticity may also be involved in repairing the brain from damage, such as from head traumas, stress, toxins, or even a lifetime of poor diet and lifestyle choices.

What is a Synapse?

Scientists currently estimate that our brain contains approximately 100 billion neurons. These neurons communicate with one another by forming synapses, which is the place where two neurons meet and connect.

However, this connection doesn’t involve direct physical contact, as it would on a circuit board, for example. Instead, each “synapse” is actually a tiny gap in between where the two neurons meet. This is where one neuron releases chemicals (neurotransmitters) in order to trigger an electrical response in the neighboring neuron.

By connecting into a series of synapses, this is how individual brain cells form signaling pathways, or “circuits”, which allows them to pass along and process information.

Synaptic plasticity refers to our brain’s ability to adjust the connections between neurons, which changes how they communicate with each other and process information.

The post Synaptic Plasticity: How It Works And Why It’s So Important appeared first on SelfHacked.

What is IBD (Ulcerative Colitis and Crohn’s)?

Crohn’s disease and ulcerative colitis (UC) are two of the most frequently diagnosed subtypes of inflammatory bowel disease (IBD).

IBD is a group of chronic inflammatory diseases characterized by inflammation and sores in the gut lining, which can result in diarrhea, abdominal pain, fatigue, fever, rectal bleeding, nutritional deficiencies, and weight loss (R).

Characteristics of Crohn’s Disease

Crohn’s may affect any portion of the gastrointestinal tract, but mostly in the ileum (lower portion of the small intestine). It involves ulcerations of all cell layers of the gut lining (R).

Crohn’s disease mainly involves Th1 and Th17 overactivation (R).

Characteristics of Ulcerative Colitis

Ulcerative colitis typically affects the colon and rectum. It involves the inflammation of the mucosal layer (innermost cell layer) of the gut (R).

It is mainly a Th2 dominant condition, although in some cases it is not clear (R).

Potential IBD Contributing Factors

None of the below factors are established causes of IBD. According to preliminary research, they may play a role in this complex disease, but the evidence is inconclusive. If you recognize one or more of these factors in your case, it doesn’t mean you have IBD. If you’re experiencing digestive issues, work with your doctor to get adequate diagnosis and treatment.

Genetics

It’s important to note that just because certain genotypes are associated with a condition or irregular lab marker, it doesn’t necessarily mean that everyone with that genotype will actually develop the condition. Many different factors, including other genetic and environmental factors, can influence the risk of IBD.

If someone has Crohn’s (CD), their identical twin with the exact same genetics has a 50% chance of developing Crohn’s (R).

If someone has ulcerative colitis (UC), their identical twin has a 10% chance of developing colitis (R).

Genetics, therefore, contributes to the development of IBD but is not the sole cause. Genes that have been associated with Crohn’s and colitis include:

1) CARD15 (CD)

CARD15 binds to the bacterial cell wall and activates NF-kB, which then stimulates the production of proinflammatory signals (R).

The post 12 IBD (Ulcerative Colitis and Crohn’s) Contributing Factors appeared first on SelfHacked.

What are T3 and T4?

The thyroid gland is located in the base of your neck and is involved in secreting important hormones T4 (thyroxine) and T3 (triiodothyronine).

T3 contains 3 iodine atoms and is created from the breakdown of T4. The breakdown of T4 is encouraged by the thyroid-stimulating hormone.

T4 is synthesized from residues of the amino acid tyrosine, found in thyroglobulin (a protein created in the thyroid). It contains 4 iodine atoms and allows the body to better control the more active T3.

If there are not enough thyroid hormones in the bloodstream, the hypothalamus will signal the pituitary gland (via TRH) to produce TSH for the thyroid to release more T3 and T4.

Reverse T3 (rT3) is the mirror image of T3. It competes with T3 and binds to the thyroid receptor but does not activate it.

Thyroid Hormones Roles and Functions

T3 and T4 affect [R]:

• Breathing
• Metabolism
• Heart rate
• The nervous system
• Bodyweight
• Muscle strength
• Menstrual cycles
• Body temperature
• Cholesterol levels
• Growth and development
• Intestinal flow
• Digestion

Metabolism

T3 changes gene expression (cellular production of certain proteins and hormones) of multiple metabolism-related genes.

These genes include PPAR-gamma, NRF1, NRF2, and other transcription factors that work with them (R).

Thyroid hormone may work in synergy with other receptors, including RXR (vitamin A receptor), or VDR (vitamin D receptor) (R).

Mitochondrial Function

T3 stimulates oxygen consumption and heat production by the mitochondria, and the production of new mitochondria (R, R).

Therefore, mitochondrial dysfunction can result in symptoms of hypothyroidism, even in the presence of healthy levels of thyroid hormones.

Immunity

Immune cells have receptors for T3, and the administration of T3 increases the size and growth of cells in the thymus (R).

In mice, T4 treatment suppresses antibody synthesis and growth of white blood cells

The post Thyroid Hormones (T3, T4): Roles, Functions, High/Low Levels appeared first on SelfHacked.

Disclaimer: DMT, an ingredient in Ayahuasca brews, is classified as a Schedule I substance. This means that it is an illegal drug with high potential for harm and no known medical uses. We highly advise against the use of DMT-containing Ayahuasca brews until future studies determine their safety and efficacy in medically-supervised and safe settings. The only aim of this post is to outline risks and research findings.

What Is Ayahuasca?

How Much Do We Know?

Ayahuasca – a chemically complex brew that exerts many psychoactive effects on users. Amazonian folk medicine claims it can enhance emotions and deep introspection and purge the body. Allegedly, shamans have been occasionally using it for spiritual purposes since pre-colonial times.

Modern science wants to understand if it can help people with mental health issues, but ayahuasca research has regulatory barriers and needs to be carefully performed because of possible side effects.

However, we know little about its impact on human health, and clinical trials are currently underway.

There are physiological and psychological risks associated with its use. Until proper safety and effectiveness trials are carried out, Ayahuasca brews will remain potentially dangerous and illegal. Thus, we currently recommend against taking them.

Historical Use

Ayahuasca (or hoasca) is a psychoactive brew made from two hallucinogenic plants (Banisteriopsis caapi and Psychotria viridis). Traditionally, this brew is used by the natives of South America for its hallucinogenic properties in their spiritual and cultural practices [R].

The brew is traditionally made by boiling the bark and stems of the two plants (Banisteriopsis caapi and Psychotria viridis) [R].

Archeological evidence suggests that the earliest use of ayahuasca was more than four thousand years ago [R].

In the 20th century, the popularity of ayahuasca began spreading around the world because of globalization and religious tourism [R].

Spiritual & Cultural Background

Essentially, ayahuasca is a hallucinogenic blend that causes psychedelic effects. Indigenous people claim that it can trigger unique out-of-body experiences. These are sometimes described as spiritual journeys that deliver some sort of advice to the users. Thus, it was strongly associated with shamanism [R].

The ayahuasca-induced state of mind is said to allow shamans to enter

The post Ayahuasca Risks, Side Effects, Experiences & New Research appeared first on SelfHacked.

What is Melatonin?

Melatonin is derived from the amino acid tryptophan and the neurotransmitter serotonin [R].

Melatonin has many important functions in the body, including:

• Influences the circadian rhythm
• Aids the immune system
• Helps eye function
• Reduces oxidative stress
• Promotes sleep
• Controls many cellular events, including synthesis of important molecules
• Protects against radiation

The pineal gland, which is nestled in the brain, makes melatonin. The quantity of melatonin in the blood depends on the time of the day. At night there is 10 to 15 times more melatonin in the blood there is in the day, which helps people sleep [R].

Melatonin is also made by many other organs in the body, especially in the stomach [R].

If sleep is interrupted by blue light exposure at night, melatonin levels decrease drastically. In addition, melatonin levels also decrease with age [R]. However, darkness does not stimulate melatonin production. It simply permits melatonin production [R].

Melatonin Receptors

Melatonin acts by interacting with two receptor proteins, MT1 and MT2 [R].

MT1 and MT2 receptors control different stages of sleep: MT1 controls deep sleep or REM sleep, and MT2 controls the stages of sleep preceding dreaming [R].

These receptors are present in a variety of organs and immune cells, suggesting that melatonin also controls the function of the immune system and other systems throughout the body [R].

Sleep and Circadian Rhythm

The circadian rhythm is like the body’s clock. It is a built-in function that controls biological processes in a roughly 24-hour cycle [R].

A central clock is located in the SCN of the anterior hypothalamus in the brain. It controls the body’s circadian rhythm. The circadian rhythm helps control the sleep-wake cycle, body temperature, and hormone production [R].

Light from the environment influences the signals sent from the SCN [R].

Under the control of the circadian rhythm, the pineal gland produces and secretes melatonin. Under normal conditions, melatonin is secreted during the night. During daylight, there are undetectable amounts in the blood [R].

While most scientists believe that melatonin can

The post 3 Benefits of Melatonin as a Sleep Aid: How does it Work? appeared first on SelfHacked.

Disclaimer: Agomelatine is not approved in the United States. The development for the US market was discontinued in October 2011. The major concern was that efficacy had not been sufficiently shown. This drug was approved in Europe in 2009 and Australia in 2010, where it can only be used with a doctor’s prescription. Discuss your symptoms with your doctor. He or she will diagnose and treat your health issues.

What is Agomelatine?

Overview

Agomelatine (Valdoxan) was developed as an atypical antidepressant on the basis that abnormal circadian rhythms may contribute to depression. This theory requires further human trials to be adequately verified [R].

A major group of antidepressant drugs is selective serotonin reuptake inhibitors (SSRIs). Unlike SSRIs, agomelatine likely activates melatonin (MT1 and MT2) receptors and blocks the 5-HT2C serotonin receptor [R].

Agomelatine is not approved for use in the United States.

This drug was undergoing several phase III clinical trials in the US. Until late 2011, agomelatine was listed as scheduled for submission to the Food Drug Administration (FDA). However, the development for the US market was discontinued and withdrawn in October 2011, when the latest clinical trial results became available [R].

Presently, agomelatine is approved in the European Union for the treatment of major depression [R, R].

Mechanism of Action

Agomelatine activates melatonergic M1 and M2 receptors and inhibits serotonergic 5-HT2C receptors [R].

Although agomelatine is molecularly similar to melatonin, it has a longer half-life [R].

The half-life of agomelatine is 2.3 hours, while melatonin has a half-life of 50 minutes. Agomelatine may also bind to melatonin receptors stronger than melatonin [R].

By blocking 5-HT2C receptors on dopaminergic and noradrenergic pathways, agomelatine may elevate dopamine and norepinephrine levels in the brain (in the prefrontal cortex but not in the limbic system). Scientists hypothesize this might improve mood and provide nootropic cognitive enhancement [R].

Researchers also suggest that agomelatine may enhance the number of spontaneously-active neurons and the bursting activity of dopaminergic neurons in the ventral tegmental brain area [R].

Research on Depression & Other Diseases

According to some theories, depression is linked to certain abnormalities in the limbic system (part of the brain involved in emotions and memory) and circadian rhythms. Scientists are researching how the following changes may be linked with depression:

• HPA Axis

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What is 5-HTP?

5-hydroxytryptophan (5-HTP) is an amino acid that serves as a precursor for the biosynthesis of serotonin and melatonin in the brain from the amino acid tryptophan.

Currently, depression is thought to caused (at least partially) by having low levels of serotonin in the brain, however, it is still not fully understood as to what exactly causes depression [R, R].

5-HTP in supplement form is extracted from the plant Griffonia simplicifolia, an African shrub.

Testing Serotonin

It is not possible to measure serotonin levels in a human brain without a brain biopsy. Indirect markers that are good indicators of serotonin levels in the brain are cortisol levels and blood or urinary HIAA levels [R, R].

Primary Benefit of 5-HTP

The people who most commonly use 5-HTP are those who struggle with depression.

Note that 5-HTP supplements have not been approved by the FDA for medical use and generally lack solid clinical research. Regulations set manufacturing standards for them but don’t guarantee that they’re safe or effective. Speak with your doctor before supplementing.

1) Depression

In small clinical studies, 5-HTP alleviated depression better than a placebo. However, more large-scale and higher quality studies are necessary to confirm the safety and effectiveness of 5-HTP [R].

The antidepressant effects of 5-HTP have been comparable to those of some conventional antidepressants [R].

The combined use of 5-HTP and SSRIs seem to have strong synergistic effects on serotonin levels in rats and humans. Therefore, some research has investigated the use of slow-release 5-HTP in combination with SSRIs [R, R, R].

In a small clinical trial involving 52 healthy male subjects, 5-HTP and an SSRI enhanced serotonin levels by 35% and 100%, respectively. Together, however, they increased serotonin by 500% [R].

Additional clinical trials are required to demonstrate the safety and effectiveness of this approach. Do not combine 5-HTP and medications without the recommendation and supervision of a doctor.

Other Potential Benefits

5-HTP is currently under investigation for several other health benefits, for which the evidence is not as strong as in the case of depression. The available research here is considered insufficient, either because the human trials are small or because only animal studies exist. Talk to your doctor before using

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What is Ginger?

What do we know?

As stated by the National Center for Complementary and Alternative Medicine (NCCIH), there is some information about the use of ginger for nausea and vomiting. Much less information is available about its other uses and purported health benefits [R].

The NCCIH points out that ginger may help relieve pregnancy-related nausea and vomiting, according to some evidence. It may also help to control nausea related to cancer chemotherapy when used in addition to conventional anti-nausea medication [R].

On the other hand, it’s unclear whether ginger is helpful for postsurgery nausea, motion sickness, rheumatoid arthritis, or osteoarthritis [R].

Today, ginger is also available as a supplement. Ginger supplements have not been approved by the FDA for medical use. In general, dietary supplements lack solid clinical research. Regulations set manufacturing standards for supplements but don’t guarantee that they’re safe or effective. Speak with your doctor before supplementing.

Where does it come from?

Ginger is a spice originated from the rhizomes of the plant Zingiber officinale. It is commonly used in many Asian, Ayurvedic, and middle eastern dishes. Ginger use dates back to 3,000 years ago in India.

In fact, ginger is one of the most commonly consumed dietary condiments in the world [R].

What is it used for?

It’s been used for thousands of years as a remedy for diverse health issues, such as colds, nausea, pain, arthritis, migraines, and high blood pressure [R].

Ginger is also an antioxidant that might fight microbes and reduce inflammation.

This spice is a relative of curcumin and cardamon, which all belong to the same plant family.

Active Components of Ginger

Over 100 active compounds have been identified in ginger, fresh or dried!

Gingerols are the major compounds in fresh ginger and less so in dry ginger.

Shogaols are produced from gingerols during the drying process and are present in higher amounts in dried ginger [R].

Ginger also contains zingerone, zerumbone, pungent oleoresins, some terpenoids and flavonoids [R].

All of these compounds are antioxidants, while some of them have anti-tumor, anti-inflammatory, pain-relieving, antimicrobial, and liver-protecting activities. However, these properties were only investigated in cell-based

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What are Retinoic Acid Receptors (RARs)?

Retinoic acid receptors (RARs) are receptors for specific forms of vitamin A, retinol, and retinoic acid (R, R).

These receptors are necessary for the body to properly sense and utilize those forms of vitamin A (R, R). As a result, the many benefits of vitamin A cannot be obtained without proper retinoic acid receptor function.

The retinoic acid receptors consist of 3 specific variations called subtypes. The three subtypes – RAR-α, RAR-β, and RAR-γ – are encoded by separate genes (R). The different subtypes are also produced and used differently in different tissues (R).

RARs are important for embryonic development, organ generation, vision, immune functions, energy production, and fertility (R).

Activation of RARs can be helpful in the treatment of disorders including type 2 diabetes, high cholesterol, immune disorders, and various cancers (R, R, R).

Other Receptors that Partner with Retinoic Acid Receptors

RARs combine with a protein called RXR (retinoid X receptors) and other nuclear receptors (PPARs, vitamin D receptor, and thyroid hormone receptors) to balance cellular energy production (R). This explains why vitamin A is important for these other receptors, i.e. PPAR, vitamin D, and thyroid hormone receptors to function well.

Health Benefits of Retinoic Acid Receptor Activity

1) Increases Metabolism

Retinoic acid is important for energy metabolism because it promotes energy usage, especially in fat cells (R). It helps activate the gene expression of cells involved in carbohydrate and fat metabolism (R).

RARs can increase lipolysis (the breakdown of fats) and help keep fat levels at a balance. Retinoic acid treatment in obese animals induces RAR production, which can lead to weight loss (R).

2) Improves Insulin Sensitivity

Retinoic acid and RAR (RAR) activity also improved insulin sensitivity and glucose tolerance in animal studies (R).

The improvements in glucose tolerance are likely explained by the retinoic acid receptor’s interactions with the cells that produce insulin, pancreatic β cells. These cells need RAR activity to produce healthy levels of insulin. Without RAR activity, the animals had a lower blood insulin level

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