Slippery Slope SUPPLEMENTS

[PeskyPeater]

I don’t know about tea tree, but I have read a lot about lavender being estrogenic. Can you post something to the contrary, because I recently dried some of my growing lavender to make lavender soda and now I have put it on hold.

Lavender and tea tree oils are not oestrogenic

 

[Peatness]

Lavender and tea tree oils are not oestrogenic

They are

 

[PeskyPeater]

They are

Take the blue pill or take the red pill..

 

[Rinse & rePeat]

“Suppressing fatty acid oxidation improves the contraction of the heart muscle and increases the efficiency of oxygen use (Chandler, et al., 2003). Various drugs are being considered for that purpose, but niacinamide is already being used to improve heart function, since it lowers the concentration of free fatty acids.“ -Ray Peat

 

[amd]

Excess nicotinamide increases plasma serotonin and histamine levels

Excess nicotinamide increases plasma serotonin and histamine levels - PubMed

Methylation, a methyl group-consuming reaction, plays a key role in the degradation (i.e., inactivation) of monoamine neurotransmitters, including catecholamines, serotonin and histamine. Without labile methyl groups, the methylation-mediated degradation cannot take place. Although high niacin...

pubmed.ncbi.nlm.nih.gov

Methylation, a methyl group-consuming reaction, plays a key role in the degradation (i.e., inactivation) of monoamine neurotransmitters, including catecholamines, serotonin and histamine. Without labile methyl groups, the methylation-mediated degradation cannot take place. Although high niacin (nicotinic acid and nicotinamide) intake, which is very common nowadays, is known to deplete the body's methyl-group pool, its effect on monoamine-neurotransmitter degradation is not well understood.

The aim of this article was to investigate the effect of excess nicotinamide on the levels of plasma serotonin and histamine in healthy subjects. Urine and venous blood samples were collected from nine healthy male volunteers before and after oral loading with 100 mg nicotinamide. Plasma N(1)-methylnicotinamide, urinary N(1)-methyl-2-pyridone-5-carboxamide (2-Py), and plasma betaine levels were measured by using high-performance liquid chromatography (HPLC). Plasma concentrations of choline, serotonin and histamine were measured using commercial kits.

The results showed that the plasma N(1)-methylnicotinamide level and the urinary excretion of 2-Py significantly increased after oral loading with 100 mg nicotinamide, which was accompanied with a decrease in the methyl-group donor betaine. Compared with those before nicotinamide load, five-hour postload plasma serotonin and histamine levels significantly increased.

These results suggest that excess nicotinamide can disturb monoamine-neurotransmitter metabolism. These findings may be of significance in understanding the etiology of monoamine-related mental diseases, such as schizophrenia and autism (a neurodevelopmental disorder.

 

[Peatness]

Thank you for posting that study @fico

 

[Rinse & rePeat]

The Amazing and Mighty Ginger

Herbal Medicine: Biomolecular and Clinical Aspects (2nd edition). Chapter 7: The Amazing and Mighty Ginger The primary purpose of this chapter is to comprehensively examine the available scientific evidence regarding ginger’s proven effectiveness in preventing or treating a variety of...

raypeatforum.com

 

[Rinse & rePeat]

“The supplements that most often help to correct diabetes-like conditions are niacinamide, thiamine, thyroid, and progesterone or pregnenolone. Vitamins D and K are clearly protective against developing diabetes, and their effects on many regulatory processes suggest that they would also help to correct existing hyperglycemia.“ -Ray Peat

 

[PeskyPeater]

Excess nicotinamide increases plasma serotonin and histamine levels

Excess nicotinamide increases plasma serotonin and histamine levels - PubMed

Methylation, a methyl group-consuming reaction, plays a key role in the degradation (i.e., inactivation) of monoamine neurotransmitters, including catecholamines, serotonin and histamine. Without labile methyl groups, the methylation-mediated degradation cannot take place. Although high niacin...

pubmed.ncbi.nlm.nih.gov

edit Here is the discussion part of that study:

Spoiler: Discussion

This study found that nicotinamide load reduced the
methyl-group pool associated with increases in plasma
serotonin and histamine levels. The present findings,
together with earlier results showing that nicotinamide
load increased plasma norepinephrine but decreased its
derivatives[7], suggest that excessive
nicotinamide could inhibit the degradation of monoamine
neurotransmitters presumably due to methyl-group pool
depletion.
In humans, nicotinamide is degraded mainly via
methylation to produce methylated metabolites, N1-
methyl nicotinamide and 2-Py[6]. Evidently, excess nic-
otinamide can increase the consumption of labile methyl
groups. Betaine serves as a methyl donor in a reaction
converting homocysteine to methionine, whereas cho-
line can be converted to betaine in the liver and kid-
ney[9]. Therefore, the levels of plasma choline and be-
taine are indicators of the size of methyl-group pool of
the body. The present findings that nicotinamide load
had a more profound inuence on plasma betaine than
choline suggest that betaine is a more effective methyl
donor than choline.
Niacin is usually classied as a B vitamin. However,
strictly speaking, it is not a vitamin because it can be
synthesized from tryptophan. As shown in Fig. 1,
tryptophan is degraded through tryptophan-kynurenine-
niacin and tryptophan-serotonin pathways. These two
pathways function together to regulate tryptophan
homeostasis. For example, an increase in nicotinamide
intake can lead to an increase in urinary excretion of
5-hydroxyindoleacetic acid, a metabolite of serotonin[10],
suggesting an increase in tryptophan degradation
through tryptophan-serotonin pathway (i.e., an increase
in serotonin synthesis). Moreover, nicotinamide may
affect methylation-mediated serotonin degradation by
competing for methyl groups. Therefore, high nicotinamide
intake may increase serotonin levels by a mechanism
of increased synthesis and decreased degradation.
Serotonin and histamine act not only as neurotrans-
mitters, but also function as important signaling
molecules in the skin, gastrointestinal tract and immune
system[11,12] on the one hand, and on the other hand,
neuropsychiatric disorders, such as autism[13] and
schizophrenia[14], are often associated with immune
abnormalities, besides disturbed monoamine-neuro-
transmitter metabolism[1,2]. The nding that nicotinamide
load increases the plasma levels of both serotonin and
histamine, suggests that excess nicotinamide load could
affect both the nervous system and the immune system.
Although not proved, high nicotinamide intake, which
is very common nowadays due to mandatory vitamin
fortication[15], may play a role in the association between
abnormal metabolism of monoamine neuro-transmitters
and immune abnormalities in neuropsychiatric disorders.
Indeed, ecological evidence has revealed an association
between the prevalence of schizophrenia and a higher
national dietary intake of refined sugar and dairy
products[3], which are vehicles for vitamin fortication[15].
As shown in Fig. 1, methylation catalyzed by distinct
methyltransferases and oxidation catalyzed by the
monoamine oxidase (MAO) are two necessary steps in
the degradation of monoamine neurotransmitters. If
methylation is interrupted due to methyl-group
depletion, the function of MAO will become increasingly
crucial to monoamine-neurotransmitter degradation.
The isoenzymes of MAO, MAO-A and MAO-B, are
X-linked enzymes[16], and the activity of MAO in
women is stronger than that of men[17]. Thus, under the
same methyl-group-pool depletion condition, men
should be more prone to mental disorders than women.
Indeed, a body of evidence has been accumulated,
suggesting that abnormal MAO-A activity is implicated
in several neuropsychiatric disorders, such as depression,
autism, and attention deficit hyperactivity disorder,
which show sexual dimorphism[18–21].
The results of this study may be of significance to
understand the etiology of mental disorders, such as
autism which is a pervasive developmental disorder
manifested in the rst 3 years of life by dysfunction in
social interaction and communication[22]. The most
consistently observed biological ndings in autism are
elevated serotonin levels in the blood and immunological
abnormalities[13]. Since autism was first described by
Kanner in 1943[23], its prevalence has dramatically
increased from 4 to 5 per 10 000 children in 1940s to
approximately 1 in 88 in the United States today[22].
Notably, the increasing prevalence of autism is accom-
panied with a significant increase in the per capita
consumption of niacin in the United States due to the
implementation of mandatory niacin fortication (i.e.,
addition of synthetic nicotinamide to grain products)[15].
Especially, infant formulas and children’s foods contain
much higher amounts of nicotinamide, for example, the
niacin (in the form of nicotinamide) contents of most
infant formulas in U.S. market range from 1 000 to
1 950 μg/100 kcal, which is more than ve times that
of human milk (ranging 164–343 μg/100 kcal[24]). Thus,
formula-feeding will increase the risk of nicotinamide
overload. This notion is supported by the observation
of high urinary excretion of niacin metabolites in
autistic subjects[25]. Thus, the present ndings that nico-
tinamide load increases the levels of plasma serotonin
and histamine imply that high nicotinamide exposure
may be a risk factor for autism, but further studies are
needed to conrm this, especially in autistic children.
In summary, excess nicotinamide increases the
plasma monoamine-neurotransmitter levels. The
present ndings provide evidence for the potential role
of nicotinamide in the metabolic disorder of monoamine
neurotransmitters

Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels

Summary​

Aim​

The present study was to compare the effects of nicotinic acid and nicotinamide on the plasma methyl donors, choline and betaine.

Methods​

Thirty adult subjects were randomly divided into three groups of equal size, and orally received purified water (C group), nicotinic acid (300 mg, NA group) or nicotinamide (300 mg, NM group). Plasma nicotinamide, N1-methylnicotinamide, homocysteine, betaine and choline levels before and 1.5-h and 3-h post-dosing, plasma normetanephrine and metanephrine concentrations at 3-h post-dosing, and the urinary excretion of N1-methyl-2-pyridone-5-carboxamide during the test period were examined.

Results​

The level of 3-h plasma nicotinamide, N1-methylnicotinamide, homocysteine, the urinary excretion of N1-methyl-2-pyridone-5-carboxamide and pulse pressure (PP) in the NM group was 221%, 3972%, 61%, 1728% and 21.2% higher than that of the control group (P < 0.01, except homocysteine and PP P < 0.05), while the 3-h plasma betaine, normetanephrine and metanephrine level in the NM group was 24.4%, 9.4% and 11.7% lower (P < 0.05, except betaine P < 0.01), without significant difference in choline levels. Similar but less pronounced changes were observed in the NA group, with a lower level of 3-h plasma N1-methylnicotinamide (1.90 ± 0.20 μmol/l vs. 3.62 ± 0.27 μmol/l, P < 0.01) and homocysteine (12.85 ± 1.39 μmol/l vs. 18.08 ± 1.02 μmol/l, P < 0.05) but a higher level of betaine (27.44 ± 0.71 μmol/l vs. 23.52 ± 0.61 μmol/l, P < 0.05) than that of the NM group.

 

[Can]

Great thread!

 

[Rinse & rePeat]

Great thread!

I appreciate you saying that.

 

[Rinse & rePeat]

“When these intrinsic corrective processes are inadequate, as in hypothyroidism, with increased estrogen and serotonin, extrinsic factors, including special foods and drugs, can reinforce the adaptive mechanisms. These “adaptogens” can sometimes restore the system to perfect functioning, other times they can merely prevent further injury. Sometimes the adaptogens are exactly like those the body normally has, but that are needed in larger amounts during stress. Coenzyme Q10, vitamin K, short-chain fatty acids, ketoacids, niacinamide, and glycine are examples of this sort--they are always present, but increased amounts can improve resistance to stress.“ -Ray Peat

 

[Sean.R]

What about Boron? And TMG (trimethylglycine)? Sorry if this has been covered already, I don't read all the threads on here

 

[Rinse & rePeat]

What about Boron? And TMG (trimethylglycine)? Sorry if this has been covered already, I don't read all the threads on here

Nobody has spoke about it here yet.

 

[Rinse & rePeat]

“Animal studies show that estrogen stunts growth, including bone growth. The high estrogen levels in girls' teen years and early twenties accounts for the fact that women's bones are lighter than men's. In rat studies, treatment with estrogen was found to enlarge the space between the jawbone and the teeth, which is a factor in periodontal disease (Elzay, 1964). Teeth are very similar to bones, so it's interesting that treating male or female rats with estrogen increases their incidence of tooth decay, and removing their gonads was found to decrease the incidence (Muhler and Shafer, 1952). Supplementing them with thyroid hormone decreased the incidence of cavities in both males and females (Bixler, et al., 1957).“ -Ray Peat

 

[Rinse & rePeat]

Thyroid hormone is essential for forming carbon dioxide. In the early 1940s, experimental rabbits were fed their standard diet, with the addition of 1% desiccated thyroid gland, which would be equivalent to about 150 grains of Armour thyroid for a person. They became extremely hypermetabolic, and couldn't eat enough to meet their nutritional needs for growth and tissue maintenance. When they died, all of their tissues weighed much less than those of animals that hadn't received the toxic dose of thyroid, except for their bones, which were larger than normal. Experiments with the thin skull bones of mice have shown that the active thyroid hormone, T3, increases the formation of bone. To increase cellular respiration and carbon dioxide production, T3 increases the activity of the enzyme cytochrome oxidase, which uses copper as a co-factor. Increased thyroid activity increases the absorption of copper from foods.“ -Ray Peat

 

[Rinse & rePeat]

“The formation of eggshell, which is mostly calcium carbonate, is analogous to the early stage of bone formation. In hot weather, when chickens pant and lower their carbon dioxide, they form thin shells. A sodium bicarbonate supplement improves the quality of the eggshell (Balnave and Muheereza, 1997; Makled and Charles, 1987). Chickens that habitually lay eggs with thinner shells have lower blood bicarbonate than those that lay thick shelled eggs (Wideman and Buss, 1985).” -Ray Peat

 

[Rinse & rePeat]

“Aspirin, which stimulates bone formation, has other thyroid-like actions, including activation of mitochondrial respiration and energy production, with an increase of cytochrome C oxidase (Cai, et al., 1996), and it lowers serotonin (Shen, et al., 2011). It also apparently protects against calcification of the soft tissues, (Vasudev, et al., 2000), though there has been surprisingly little investigation of that. "Aspirin can promote trabecular bone remodeling, improve three-dimensional structure of trabecular bone and increase bone density of cancellous in osteoporotic rats by stimulating bone formation. It may become a new drug for the treatment of osteoporosis" (Chen, et al., 2011).“ -Ray Peat

 

[Rinse & rePeat]

“Niacin amide is a nutrient that inhibits the release of fatty acids, and it also activates phagocytic activity and lowers phosphate. It protects against the development of scars in spinal cord injuries, facilitates recovery from traumatic brain injury, and accelerates healing generally. While it generally supports immunity, it’s protective against autoimmunity. It can cause tumor cells to either mature or disintegrate, but it prolongs the replicative life of cultured cells, and protects against excitotoxicity.“ -Ray Peat

 

[Rinse & rePeat]

“According to the coroner's documents, Lori McClintock's death resulted from "adverse effects of white mulberry leaf ingestion." Ingestion of the tree leaves caused gastroenteritis (inflammation of the stomach and intestines) that led to dehydration, which caused her death. The coroner's documents noted that McClintock's body had elevated levels of nitrogen, sodium, and creatinine, which independent pathologists confirmed to KHN were signs of dehydration. The cause of death listed on her death certificate was updated from "pending" to an accident.

Like many herbal remedies, white mulberry is said to be useful in treating various health conditions—with little to no evidence. The most common is diabetes. Studies have suggested that the tree, native to China, contains anti-diabetic compounds that can lower blood glucose levels in diabetic mice. But white mulberry is also said to help with high cholesterol, high blood pressure, obesity, weight loss, the common cold, joint pain, and arthritis, among other conditions.

Lingering questions

It's unclear why McClintock was ingesting white mulberry leaves—or how, exactly. Tom McClintock mentioned that his wife was "carefully dieting," which might indicate she was taking the leaves for weight loss. Common ways to consume mulberry leaves include extracts, powders, and teas. But, according to the coroner's report, McClintock had a "partially intact" white mulberry leaf in her stomach at the time of death, suggesting she had ingested fragments or whole leaves.

It's also unclear why she had such a severe reaction to the leaves. KHN notes that no deaths linked to white mulberry have been reported to poison control centers in the last 10 years. While there have been nearly 150 poison control reports of ingestion in that time, most were related to accidental intake by children.“

An herbal remedy caused the death of CA congressman’s wife

A bit of undigested white mulberry leaf was found in the woman's stomach.

www.google.com