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Formaldehyde in Foods

#61 · March 3, 2022, 2:20 am

@beata-2 sounds like a good plan. I’m all in favour of abandoning biochemistry and focusing on ‘higher’ levels of healing. I think it’s the way to better health. However, I’m an ex research scientist and find the biochemistry interesting 😀 In my studying of NAD deficiency, two things that modulate the pathway that ‘steals’ it away are nitric oxide and oxytocin! Being happy can do a lot for biochemistry. Simple things can have a big impact.

I’ve been re-visiting Dino’s posts on breathing. Anyone who hasn’t seen them may get valuable information by searching for them. He emphasises the importance of the right breathing for detoxification. I came across a comment by Grant saying he had research showing that formaldehyde was detoxed by breath and that his steep cycle to work could have been very helpful for his detox. Getting the basics right is so important.

puddleduck, Audrey and 5 other users have reacted to this post.

#62 · September 5, 2022, 4:36 am

Quote from MaryAnn on December 13, 2019, 9:44 am

I am also quite gluten intolerant, so much so that I even have a problem with white rice. After giving up rice for good I found a research article that tested gluten reactivity in other grains and foods, which found rice, millet and corn have a slight reactivity to a gluten antibody. They also tested buckwheat and found no reactivity.

I have been eating buckwheat for about 5 months and have not had any problems. The white rice caused a slow buildup of inflammation and gave me a case of vertigo (BPPV). White rice also affected my son, worsening his ADHD symptoms. "Natural flavors" also seem to make his ADHD and depression worse.

It's a long slow process figuring out what works and what doesn't. It's so wonderful to have this discussion/support group for help! Here's wishing us all good health!

I also suffer from the same allergy to rice, but I want to know how you deal with the high level of oxalate in buckwheat before I start it

#63 · February 26, 2023, 6:05 am

Quote from tim on February 26, 2023, 6:05 am
I recommend reading this article in full but here are some excerpts.

Metabolic Methanol: Molecular Pathways and Physiological Roles

Yuri L. Dorokhov, Anastasia V. Shindyapina, Ekaterina V. Sheshukova, and Tatiana V. Komarova
01 APR 2015

Abstract
Methanol has been historically considered an exogenous product that leads only to pathological changes in the human body when consumed. However, in normal, healthy individuals, methanol and its short-lived oxidized product, formaldehyde, are naturally occurring compounds whose functions and origins have received limited attention. There are several sources of human physiological methanol. Fruits, vegetables, and alcoholic beverages are likely the main sources of exogenous methanol in the healthy human body. Metabolic methanol may occur as a result of fermentation by gut bacteria and metabolic processes involving S-adenosyl methionine. Regardless of its source, low levels of methanol in the body are maintained by physiological and metabolic clearance mechanisms. Although human blood contains small amounts of methanol and formaldehyde, the content of these molecules increases sharply after receiving even methanol-free ethanol, indicating an endogenous source of the metabolic methanol present at low levels in the blood regulated by a cluster of genes. Recent studies of the pathogenesis of neurological disorders indicate metabolic formaldehyde as a putative causative agent. The detection of increased formaldehyde content in the blood of both neurological patients and the elderly indicates the important role of genetic and biochemical mechanisms of maintaining low levels of methanol and formaldehyde.

I. INTRODUCTION
Robert Boyle first described wood spirits, or methanol, as the “sowrish spirit” of boxwood pyrolysis in 1661 (44), and the function of methanol in plant and animal life has since been unclear. In higher plants, cell wall (CW) pectin methylesterase (PME) produces methanol by pectin demethylation (248). Terrestrial atmospheric methanol emission comes from volcanoes, H2 and CO2 generation within seafloor hydrothermal systems, and biomass combustion, but PME-mediated emission from plants is most likely the largest source of methanol in the atmosphere (512). Methanol accumulates in the intercellular air space or the liquid pool when the stomata close at night, and a large quantity of methanol is released when the stomata open in the morning (193). Gaseous methanol was traditionally considered to be a biochemical “waste product.” However, the effects of PME-generated plant methanol (“emitters”) on plant defensive reactions (“receivers”) and plant-animal communication have recently been shown (111, 112).

In humans, methanol is considered to be a poison because alcohol dehydrogenase 1b (ADH1b) mainly metabolizes methanol into toxic formaldehyde (63). Methanol itself is not toxic to animal cells; however, formaldehyde is responsible for carcinogenesis and age-related damage to neurons in the brain (472).

Until recently, it was believed that the trace amounts of methanol and formaldehyde in the blood of healthy people came only from the consumption of fake or low-quality alcoholic beverages. However, recent data have indicated that methanol and short-lived formaldehyde are actually naturally occurring compounds in normal, healthy human individuals (413). There are several sources of physiological methanol in humans (Figure 1). Fruits, vegetables, and alcoholic beverages are likely to be the main sources of exogenous methanol in the healthy humans. More than 50 years ago (126), two other sources were suggested: anaerobic fermentation by gut bacteria (38, 208, 209, 418) and the transformation of S-adenosyl methionine (SAM) to methanol by certain metabolic processes (16). Although human blood contains small amounts of methanol and formaldehyde, their contents are sharply increased after receiving even methanol-free ethanol (413). This indicates the existence of an endogenous source of low levels of metabolic methanol in the blood, the regulation of which is controlled by a cluster of genes (246, 413).

Figure 1.
Overview of physiological methanol biogenesis. This figure summarizes the data on methanol. The methyl group donor SAM is synthesized via the catalytic activity of methionine adenosyltransferase, which transfers the adenosyl group of ATP to methionine (step 1). S-adenosyl homocysteine is formed after SAM transfers a methyl group to a methyl acceptor (step 2) such as DNA; thus methanol is involved in gene regulation (step 11). Methyl esters such as carboxyl methyl esters are unstable and are readily hydrolyzed in neutral and basic pH conditions or by methylesterase to produce methanol (step 3). Other sources of methanol include the human diet, which supplies the methanol-generating pectin/PME complex via fruits and vegetables (steps 4 and 5), aspartame as a synthetic nonnutritive sweetener (step 6) and alcoholic beverages (step 7). The human gut microbiota is a putative methanol source (step 8) and takes part in the generation of human endogenous ethanol (step 9). We suggest that endogenous and dietary methanol may be involved in the regulation of genes involved in the metabolic clearance of methanol (step 10). The first stage of the oxidative metabolism of methanol is executed by the catalase-H2O2 system (step 12), cytochrome P450 (CYP2E1)-mediated oxidation (step 13) and, mainly, the alcohol dehydrogenase I (ADH1) class of enzymes (step 14). Although ADH1 converts methanol into toxic formaldehyde, physiological ethanol in the bloodstream substantively prevents all formaldehyde production from endogenous and dietary methanol in humans (step 15).

The consumption of vegetables such as leafy salads results in increased blood methanol contents, by ∼30% (112). The ingestion of pectin, fruits with different degrees of ripeness, or fruit juices leads to the rise of the methanol content of exhaled air (126, 451, 474) and blood (278). This occurs mainly due to the demethylation of pectin contained in vegetables by PME, which is also present in the plant CW. When citrus pectin in the presence of PME activity was administered to mice, their blood methanol levels increased by more than 15-fold compared with those administered pectin without PME activity just 10 min after ingestion (112). Pectin demethylation is also believed to occur in the gut by the gut microbiota (418), as some strains of gut-inhabiting bacteria possess pectolytic enzymes. However, the administration of pectin containing no active PME in the gastrointestinal tract of mice did not lead to significant differences in the concentrations of methanol in their blood compared with the control; thus it can be concluded that the contribution of the intestinal microflora in methanol generation from pectin is rather low compared with the methanol production from ingested plant food by PME (112).

C. Formaldehyde and Hangover
Methanol and formaldehyde are known to participate in the development of a hangover, known for unpleasant sensations and uncomfortable “morning after” symptoms in people following excessive ethanol intake (373, 377). Hangovers after binge drinking are likely more common in the young than in older aged persons (462). Among hangover causes, which include imbalances in the immune system (373), effects of dehydration such as headaches (415) and sleep disturbances, acetaldehyde accumulation, dysregulated cytokine pathways, and hormonal alterations (487, 510), the metabolism of methanol and production of formaldehyde are likely the most important (28, 446). The first support for the contribution of methanol to hangovers comes from data showing that brandies and whiskeys, which are more frequently associated with the development of a hangover, contain the highest methanol concentrations. The first excellent study of methanol metabolism and hangover found that methanol accumulated in the blood of alcoholic subjects during a 10- to 15-day period of chronic ethanol intake (299). The disappearance of blood methanol lagged behind the linear disappearance of ethanol by ∼6–8 h, and complete clearance of blood methanol took several days. Importantly, the accumulation and clearance patterns of methanol and ethanol were similar in subjects who consumed either whisky (bourbon) with a high methanol content or grain alcohol with low methanol content. The authors suggested that methanol accumulates in the blood as a result of the well-known competitive inhibition of ADH by ethanol (263) and the presence of endogenous methanol (413), which may contribute to the hangover severity (299). An experimental study with healthy subjects who consumed red wine containing 100 mg/l of methanol also showed that elevated blood methanol levels persisted for several hours after the ethanol was metabolized and that this corresponded to the time course of hangover symptoms (212, 213). The half-life of methanol in healthy men during a hangover was estimated to be 142 min. This indicates that elevated methanol concentrations in the blood persist for ∼12 h (213). The author suggested that methanol lingers after ethanol levels drop because ethanol competitively inhibits methanol metabolism. Ethanol readministration (“hair-of-the-dog” drinking) (377) fends off the hangover effects that may be based on the ability of ethanol to block methanol metabolism, thereby slowing the production of formaldehyde and formic acid (213, 413).

D. Effect of Alcoholic Beverages on the Cardiovascular System: U-Shape
The consumption of ethanol has an effect on the cardiovascular system in humans and can cause coronary heart disease (CHD) (333, 355). A plethora of epidemiological evidence has demonstrated a J- or U-shaped association between alcoholic beverages consumption and all-cause mortality, as well as cardiovascular morbidity and mortality. On the other hand, moderate alcoholic beverages consumption was inversely associated with CDH mortality (144, 147, 241, 305, 335, 337, 366, 402). According to the Dietary Guidelines for Americans (314), moderate alcoholic beverages consumption is considered an intake of no more than 1 drink per day for women and no more than 2 drinks per day for men, where 1 drink is equal to ∼12 g ethanol. Moderate ethanol consumption also has a beneficial effect in reducing the risk of vascular disorders of the brain. Heavy alcoholic beverage consumption increases the relative risk of any type of stroke, whereas light or moderate ethanol consumption may be protective against ischemic stroke (241, 366). The mechanism of this phenomenon is not completely understood. Numerous hypotheses have been proposed to explain the benefit of light-to-moderate ethanol intake on the heart and brain, including an increase of high-density lipoprotein cholesterol (47) and the promotion of antioxidant effects with the participation of a protein kinase B/nuclear factor (erythroid-derived 2)-like 2-dependent mechanism (77, 241, 494). A recent study also suggested the involvement of the ADH1b gene in the U-shaped curve. A survey of over 260,000 individuals showed that carriers of the rs1229984 A-allele (ADH1B*2, Table 3) with a 100-fold increase in β2-ADH turnover (215, 308) consumed less ethanol and had a reduced frequency of coronary heart disease compared with noncarriers of this allele (184). In the search for mechanisms to explain the U-shaped relationship between ethanol consumption levels and coronary heart disease, researchers have focused on methanol and its oxidation product, formaldehyde. Recently, formaldehyde was hypothesized to participate in the process (322). The proposed mechanism relies on the fact that the common ADH1b enzyme carries out one-phase catabolism of methanol and ethanol. Moderate ethanol consumption competitively inhibits the conversion of methanol to formaldehyde, thus reducing the endogenous formaldehyde content in the organs. Another possible mechanism for the beneficial effects of moderate ethanol intake was indicated by the results of a study in rats showing that ALDH2 oxidizes aldehydes, including formaldehyde, and may serve as a potential endogenous neuroprotective target and a promising therapeutic strategy for the management of stroke (438). Ethanol administration activated ALDH2 and enhanced the detoxification of aldehydes (161). The study of ALA also indicated that ALDH2 participates in the formaldehyde and acetaldehyde detoxification process (116, 171a, 285, 310).

Methanol itself is not toxic to human cells; however, its oxidative product, formaldehyde, is a toxin that is believed to play a role in carcinogenesis and age-related neuronal damage in the brain (472). Although formaldehyde is primarily produced by the oxidation of methanol, there are several sources of metabolic formaldehyde, including SSAO-mediated oxidative deamination and the removal of methyl groups from lysine residues in histones catalyzed by histone demethylases.

I recommend reading this article in full but here are some excerpts.

Metabolic Methanol: Molecular Pathways and Physiological Roles

Yuri L. Dorokhov, Anastasia V. Shindyapina, Ekaterina V. Sheshukova, and Tatiana V. Komarova
01 APR 2015

Abstract
Methanol has been historically considered an exogenous product that leads only to pathological changes in the human body when consumed. However, in normal, healthy individuals, methanol and its short-lived oxidized product, formaldehyde, are naturally occurring compounds whose functions and origins have received limited attention. There are several sources of human physiological methanol. Fruits, vegetables, and alcoholic beverages are likely the main sources of exogenous methanol in the healthy human body. Metabolic methanol may occur as a result of fermentation by gut bacteria and metabolic processes involving S-adenosyl methionine. Regardless of its source, low levels of methanol in the body are maintained by physiological and metabolic clearance mechanisms. Although human blood contains small amounts of methanol and formaldehyde, the content of these molecules increases sharply after receiving even methanol-free ethanol, indicating an endogenous source of the metabolic methanol present at low levels in the blood regulated by a cluster of genes. Recent studies of the pathogenesis of neurological disorders indicate metabolic formaldehyde as a putative causative agent. The detection of increased formaldehyde content in the blood of both neurological patients and the elderly indicates the important role of genetic and biochemical mechanisms of maintaining low levels of methanol and formaldehyde.

I. INTRODUCTION
Robert Boyle first described wood spirits, or methanol, as the “sowrish spirit” of boxwood pyrolysis in 1661 (44), and the function of methanol in plant and animal life has since been unclear. In higher plants, cell wall (CW) pectin methylesterase (PME) produces methanol by pectin demethylation (248). Terrestrial atmospheric methanol emission comes from volcanoes, H2 and CO2 generation within seafloor hydrothermal systems, and biomass combustion, but PME-mediated emission from plants is most likely the largest source of methanol in the atmosphere (512). Methanol accumulates in the intercellular air space or the liquid pool when the stomata close at night, and a large quantity of methanol is released when the stomata open in the morning (193). Gaseous methanol was traditionally considered to be a biochemical “waste product.” However, the effects of PME-generated plant methanol (“emitters”) on plant defensive reactions (“receivers”) and plant-animal communication have recently been shown (111, 112).

In humans, methanol is considered to be a poison because alcohol dehydrogenase 1b (ADH1b) mainly metabolizes methanol into toxic formaldehyde (63). Methanol itself is not toxic to animal cells; however, formaldehyde is responsible for carcinogenesis and age-related damage to neurons in the brain (472).

Until recently, it was believed that the trace amounts of methanol and formaldehyde in the blood of healthy people came only from the consumption of fake or low-quality alcoholic beverages. However, recent data have indicated that methanol and short-lived formaldehyde are actually naturally occurring compounds in normal, healthy human individuals (413). There are several sources of physiological methanol in humans (Figure 1). Fruits, vegetables, and alcoholic beverages are likely to be the main sources of exogenous methanol in the healthy humans. More than 50 years ago (126), two other sources were suggested: anaerobic fermentation by gut bacteria (38, 208, 209, 418) and the transformation of S-adenosyl methionine (SAM) to methanol by certain metabolic processes (16). Although human blood contains small amounts of methanol and formaldehyde, their contents are sharply increased after receiving even methanol-free ethanol (413). This indicates the existence of an endogenous source of low levels of metabolic methanol in the blood, the regulation of which is controlled by a cluster of genes (246, 413).

Figure 1.
Overview of physiological methanol biogenesis. This figure summarizes the data on methanol. The methyl group donor SAM is synthesized via the catalytic activity of methionine adenosyltransferase, which transfers the adenosyl group of ATP to methionine (step 1). S-adenosyl homocysteine is formed after SAM transfers a methyl group to a methyl acceptor (step 2) such as DNA; thus methanol is involved in gene regulation (step 11). Methyl esters such as carboxyl methyl esters are unstable and are readily hydrolyzed in neutral and basic pH conditions or by methylesterase to produce methanol (step 3). Other sources of methanol include the human diet, which supplies the methanol-generating pectin/PME complex via fruits and vegetables (steps 4 and 5), aspartame as a synthetic nonnutritive sweetener (step 6) and alcoholic beverages (step 7). The human gut microbiota is a putative methanol source (step 8) and takes part in the generation of human endogenous ethanol (step 9). We suggest that endogenous and dietary methanol may be involved in the regulation of genes involved in the metabolic clearance of methanol (step 10). The first stage of the oxidative metabolism of methanol is executed by the catalase-H2O2 system (step 12), cytochrome P450 (CYP2E1)-mediated oxidation (step 13) and, mainly, the alcohol dehydrogenase I (ADH1) class of enzymes (step 14). Although ADH1 converts methanol into toxic formaldehyde, physiological ethanol in the bloodstream substantively prevents all formaldehyde production from endogenous and dietary methanol in humans (step 15).

The consumption of vegetables such as leafy salads results in increased blood methanol contents, by ∼30% (112). The ingestion of pectin, fruits with different degrees of ripeness, or fruit juices leads to the rise of the methanol content of exhaled air (126, 451, 474) and blood (278). This occurs mainly due to the demethylation of pectin contained in vegetables by PME, which is also present in the plant CW. When citrus pectin in the presence of PME activity was administered to mice, their blood methanol levels increased by more than 15-fold compared with those administered pectin without PME activity just 10 min after ingestion (112). Pectin demethylation is also believed to occur in the gut by the gut microbiota (418), as some strains of gut-inhabiting bacteria possess pectolytic enzymes. However, the administration of pectin containing no active PME in the gastrointestinal tract of mice did not lead to significant differences in the concentrations of methanol in their blood compared with the control; thus it can be concluded that the contribution of the intestinal microflora in methanol generation from pectin is rather low compared with the methanol production from ingested plant food by PME (112).

C. Formaldehyde and Hangover
Methanol and formaldehyde are known to participate in the development of a hangover, known for unpleasant sensations and uncomfortable “morning after” symptoms in people following excessive ethanol intake (373, 377). Hangovers after binge drinking are likely more common in the young than in older aged persons (462). Among hangover causes, which include imbalances in the immune system (373), effects of dehydration such as headaches (415) and sleep disturbances, acetaldehyde accumulation, dysregulated cytokine pathways, and hormonal alterations (487, 510), the metabolism of methanol and production of formaldehyde are likely the most important (28, 446). The first support for the contribution of methanol to hangovers comes from data showing that brandies and whiskeys, which are more frequently associated with the development of a hangover, contain the highest methanol concentrations. The first excellent study of methanol metabolism and hangover found that methanol accumulated in the blood of alcoholic subjects during a 10- to 15-day period of chronic ethanol intake (299). The disappearance of blood methanol lagged behind the linear disappearance of ethanol by ∼6–8 h, and complete clearance of blood methanol took several days. Importantly, the accumulation and clearance patterns of methanol and ethanol were similar in subjects who consumed either whisky (bourbon) with a high methanol content or grain alcohol with low methanol content. The authors suggested that methanol accumulates in the blood as a result of the well-known competitive inhibition of ADH by ethanol (263) and the presence of endogenous methanol (413), which may contribute to the hangover severity (299). An experimental study with healthy subjects who consumed red wine containing 100 mg/l of methanol also showed that elevated blood methanol levels persisted for several hours after the ethanol was metabolized and that this corresponded to the time course of hangover symptoms (212, 213). The half-life of methanol in healthy men during a hangover was estimated to be 142 min. This indicates that elevated methanol concentrations in the blood persist for ∼12 h (213). The author suggested that methanol lingers after ethanol levels drop because ethanol competitively inhibits methanol metabolism. Ethanol readministration (“hair-of-the-dog” drinking) (377) fends off the hangover effects that may be based on the ability of ethanol to block methanol metabolism, thereby slowing the production of formaldehyde and formic acid (213, 413).

D. Effect of Alcoholic Beverages on the Cardiovascular System: U-Shape
The consumption of ethanol has an effect on the cardiovascular system in humans and can cause coronary heart disease (CHD) (333, 355). A plethora of epidemiological evidence has demonstrated a J- or U-shaped association between alcoholic beverages consumption and all-cause mortality, as well as cardiovascular morbidity and mortality. On the other hand, moderate alcoholic beverages consumption was inversely associated with CDH mortality (144, 147, 241, 305, 335, 337, 366, 402). According to the Dietary Guidelines for Americans (314), moderate alcoholic beverages consumption is considered an intake of no more than 1 drink per day for women and no more than 2 drinks per day for men, where 1 drink is equal to ∼12 g ethanol. Moderate ethanol consumption also has a beneficial effect in reducing the risk of vascular disorders of the brain. Heavy alcoholic beverage consumption increases the relative risk of any type of stroke, whereas light or moderate ethanol consumption may be protective against ischemic stroke (241, 366). The mechanism of this phenomenon is not completely understood. Numerous hypotheses have been proposed to explain the benefit of light-to-moderate ethanol intake on the heart and brain, including an increase of high-density lipoprotein cholesterol (47) and the promotion of antioxidant effects with the participation of a protein kinase B/nuclear factor (erythroid-derived 2)-like 2-dependent mechanism (77, 241, 494). A recent study also suggested the involvement of the ADH1b gene in the U-shaped curve. A survey of over 260,000 individuals showed that carriers of the rs1229984 A-allele (ADH1B*2, Table 3) with a 100-fold increase in β2-ADH turnover (215, 308) consumed less ethanol and had a reduced frequency of coronary heart disease compared with noncarriers of this allele (184). In the search for mechanisms to explain the U-shaped relationship between ethanol consumption levels and coronary heart disease, researchers have focused on methanol and its oxidation product, formaldehyde. Recently, formaldehyde was hypothesized to participate in the process (322). The proposed mechanism relies on the fact that the common ADH1b enzyme carries out one-phase catabolism of methanol and ethanol. Moderate ethanol consumption competitively inhibits the conversion of methanol to formaldehyde, thus reducing the endogenous formaldehyde content in the organs. Another possible mechanism for the beneficial effects of moderate ethanol intake was indicated by the results of a study in rats showing that ALDH2 oxidizes aldehydes, including formaldehyde, and may serve as a potential endogenous neuroprotective target and a promising therapeutic strategy for the management of stroke (438). Ethanol administration activated ALDH2 and enhanced the detoxification of aldehydes (161). The study of ALA also indicated that ALDH2 participates in the formaldehyde and acetaldehyde detoxification process (116, 171a, 285, 310).

Methanol itself is not toxic to human cells; however, its oxidative product, formaldehyde, is a toxin that is believed to play a role in carcinogenesis and age-related neuronal damage in the brain (472). Although formaldehyde is primarily produced by the oxidation of methanol, there are several sources of metabolic formaldehyde, including SSAO-mediated oxidative deamination and the removal of methyl groups from lysine residues in histones catalyzed by histone demethylases.

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Formaldehyde in Foods

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