Is Inositol Helpful Overall Or Not?

[ddjd]

I take it for PCOS. An unexpected bonus is that it helps with constipation (but doesn't cause diarrhea).

It's important to take a little D-chiro-inositol with myo-inositol or you could get yourself an imbalance and throw everything off. The normal ratio is 40:1 myo-inositol to D-chiro-inositol.

I take Ovasitol, it has zero exipients or fillers. The taste is sweet, you can mix with anything.

Yeah inositol pure powder actually tastes amazing. How much do you dose?

 

[alywest]

Reduction in triglycerides and ldl cholesterol

Increased circulating E2

It seems like the lion's share of research regarding myo and d-chiro inositol is done on women with PCOS or with ovulation failure, so it's difficult to say if it's really beneficial for everyone else. It seems to improve insulin sensitivity and lower testosterone in women with PCOS, but these women are supposedly "hyperandrogenic." So it maybe that it is balancing out the excess for them, but in other people it might have other effects.

 

[alywest]

Myo-inositol content of common foods: development of a high-myo-inositol diet

Spoiler: By expanding I agree that my mobile device will crash

View attachment 11087
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There's something odd here, the values of fruits and their fresh juices aren't matching.

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for the authors, finally researchers that know how to properly compose this kind of table in a way that has practival value for humanoids.

This is great, thanks! Perhaps the fact that I've been craving a lot of the foods higher on the list shows that I am deficient or could at least benefit from more myo-inositol. What do you think about the supposed necessity to take d-chiro inositol along with it?

 

[alywest]

Effect of Myoinositol and Antioxidants on Sperm Quality in Men with Metabolic Syndrome

Hormone and metabolic profiles as well as semen parameters were evaluated in the relevant study at the beginning and after three months of therapy. The patients were treated by a dietary supplement administered twice a day containing 1 g MI, 30 mg L-carnitine, L-arginine and vitamin E, 55 μg selenium, and 200 μg folic acid (Andrositol, Lo.Li. Pharma s.r.l., Rome).

In regard of hormone profile, only FSH levels were not affected by the supplementation, whilst plasma, E2, and SHBG levels decreased significantly after the treatment ( and , resp.). Following the treatment, authors observed that a statistically significant increase in LH levels (), as well as in free () and total testosterone levels (), occurred. Table 2 shows the semen characteristics evaluated before and after Andrositol administration.

 

[Amazoniac]

This is great, thanks! Perhaps the fact that I've been craving a lot of the foods higher on the list shows that I am deficient or could at least benefit from more myo-inositol. What do you think about the supposed necessity to take d-chiro inositol along with it?

I know little about inositol, but it doesn't seem to be a good idea to supplement a lot of B-vitamins (including choline) without it.

- Nutritional and Acquired Deficiencies in Inositol Bioavailability. Correlations with Metabolic Disorders

"Inositol deficiency registered some interest during recent decades, mostly in an attempt to explain the therapeutic mechanism of lithium, credited to act by inducing a depletion of cellular inositol [65].

However, inositol deficiency may arise through a plethora of different mechanisms—including reduced food-dependent intake, increased catabolism, and excretion, decreased biosynthesis, inhibition of intestinal and cellular uptake—and can significantly affect several human pathological conditions [66]. In addition, despite myo-Ins deficiency being ascertained in different animal species [67], requirements for dietary inositol in man have still not been explicitly assessed. In addition, reliable estimation can be difficult because dietary necessities may be higher depending on the person’s age, the long-term use of antibiotics, or the regular consumption of a high amount of coffee [68] or other unknown diet components."

"Living organisms—from yeast to mammals—can synthetize myo-Ins up to 4–5 g/daily. This estimation indicates that the overall myo-Ins daily requirement in basal conditions (including both external sources and endogenous synthesis), should not be below the threshold value of 5–6 g. Yet, as the biosynthetic capability hugely varies among different tissues and independent of changing functional requirements (morphogenesis, sperm production, etc.), it can be hypothesized that myo-Ins biosynthesis should change accordingly."

"Cellular inositol uptake is [] decreased in the presence of high or even normal glucose concentrations. Namely, hyperglycemia induces myo-Ins depletion in nervous tissues, via competitive inhibition of sodium-dependent myo-Ins uptake [107]. By considering the structural similarities between myo-Ins and glucose, this result is far from surprising."

"Glucose may also induce myo-Ins depletion even through a biochemical pathway switching. Indeed, in diabetic patients, inositol depletion could arise due to the activation of the polyol pathway (glucose-sorbitol pathway), whereby glucose is first converted to sorbitol by aldose reductase and then to fructose by sorbitol dehydrogenase [110]." "Increased conversion of glucose into sorbitol significantly raises the intracellular osmolarity. To counteract that harmful event, cells actively inhibit the uptake of other relevant osmolytes (like inositol) and favor their cytosolic depletion, by downregulating the expression of specific carriers at the transcriptional level [112]."

"Increase in extracellular glucose (within the range mimicking the one observed in diabetes) caused marked decrease in the synthesis of phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol [115], resulting in chronic elevation of diacylglycerol (DAG), the chief physiological activator of protein kinase C (PKC) [116]. Moreover, the activation of the polyol pathway and the concomitantly reduction in cellular myo-Ins content can promote the oxidation of the NADPH/NADP+ and reduces the NADH/NAD+ redox couples, thereby perturbing a range of other adenine nucleotide-linked reactions. In diabetes, oxidation of NADPH/NADP+ may enhance susceptibility to oxidative tissue damage through depletion of reduced glutathione [117].

These findings not only provide further support to the hypothesis for which peripheral nerve integrity is highly dependent on the inositol-pathways [118], but also strengthen the link between hyperglycemia and deregulated inositol metabolism."

"Glucose-dependent depletion of cellular inositol storage has received further confirmation by a compelling body of observations. Hyperglycemia has been associated with an intracellular myo-inositol depletion in some tissues, especially in those susceptible of developing diabetes complications [119]. Moreover, hyperglycemia and insulin-resistance modify the relative proportion—namely by modulating the myo-Ins/d-chiro-Ins ratio—in which different inositol isomers are represented in different tissues [120]. In experimentally induced diabetes, inositol depletion—resulting from both cellular depletion and increased inositol urinary excretion—is an early marker of hyperglycemia and insulin resistance [102].

Myo-inositol depletion, in turn, may worsen insulin resistance and diabetes complication, including disturbances in cellular redox and free radical defense, increased oxidative glycation stress [121,122], and renal function. Conversely, myo-Ins supplementation improves several diabetes symptoms, as well as metabolic markers in a wide range of pathological conditions [123,124]."

"Inositol is chiefly catabolized in the kidney, where the enzyme myo-inositol oxygenase (MIOX) specifically metabolizes myo-Ins through the glucuronate-xylulose pathway." "Nephrectomy in animals impairs myo-Ins degradation, while renal failure is associated with significant abnormalities in myo-Ins metabolism and both inositol plasma and urinary levels [127]."

"Previous studies on animal models of diabetes documented an increased urinary loss involving only one isomer (myo-Ins or d-Chiro-Ins) [129,130], or both [128]. Similarly, in humans, increased urinary myo-inositol has been consistently demonstrated in both type 2 diabetes [120,131,132], and type 1 diabetes [133]."

"These findings suggest that deregulation of glucose metabolism will trigger abnormalities in myo-Ins metabolism and can increase the production of inositol-dependent toxic metabolites, which ultimately will damage renal function and promote inositol urinary loss. Therefore, it is likely that during hyperglycemia, insulin resistance and/or hypertension, changes in kidney metabolism are directly responsible for increased inositol loss, including both myo-Ins and d-Chiro-Ins isomers."​

- Inositol phospholipids in membrane function

--

From a consideration of the radiological findings it is our opinion that in each of the sets, other than set 5 (which received both inositol and pantothenic acid) there are features in common suggesting that the two factors, inositol and pantothenic acid, are both associated with the maintenance of gastro-intestinal normalcy. That other factors, such as pyridoxine, may influence the general picture is illustrated by the hypotonicity of sets 1 and 4. The striking similarity of pantothenic acid and inositol deficiencies in their effect on the gastro-intestinal tract is to be emphasized and suggests the presence of an interdependence of the two factors. The same features characterize the picture if either is absent from the diet. These features are:
1. Increased gastric emptying time with pylorospasm.
2. Marked segmentation of both the small and the
large intestine.
3. General picture of hypertonicity with hypomotility.
4. Alternation of ribbon-like segments with dilated
loops.
5. Frequent formation of gas.
6. Fluid levels.

Physicians who believe vitamins belong only in the diet and that the diet can always be depended on to supply them in adequate quantity, nevertheless, have no hesitancy in violating this belief with "lipotropics," for these by some miracle of logic are treated solely as drugs. But choline, inositol, pyridoxine and cyanocobalamine (vitamin B12) are all members of the vitamin B complex and methionine is an amino acid: their use therefore entails "nutritional" therapy. Furthermore other nutritional factors, identified and unidentified, also play a part in lipoid metabolism and the "lipotropic" factors have many other functions beside their role in the degradation, deposition and distribution of neutral fats, phospholipids and cholesterol.

Realization of these facts is important to adequate therapy of nutritional disturbances involving such disorders. The use of large doses of choline, inositol or methionine alone may ultimately actually aggravate the basic nutritional defect. A balanced and complete regime containing moderate doses of these substances together with all the other recognized essential factors and a satisfactory natural source, invariably produces a superior therapeutic result.

At times, however, the administration of one member may produce a deficiency syndrome. This curious finding occurred when six members of the B complex group (thiamine, riboflavin, pyridoxine, niacin, choline and pantothenic acid) were fed with inositol. A syndrome developed which could only be prevented by para-aminobenzoic acid, but if paraaminobenzoic acid were added to these same six vitamins, inositol deficiency resulted.19

A comparison of the lipotropic effects of choline, lipocaic [raw pancreatic alcoholic extractus], and inositol been made with various types of fatty livers caused by diet in rats. Choline is effective for thiamine fatty livers, and partially effective with cholesterol fatty livers, but shows little activity with biotin fatty livers. Against this last type both inositol and lipocaic are active. Lipocaic apparently differs from inositol in being ineffective against fatty livers caused by feeding cholesterol with a high fat diet. Inositol shows no activity with thiamine fatty livers; the addition of other B vitamins permits inositol to be lipotropic.

 

[alywest]

I know little about inositol, but it doesn't seem to be a good idea to supplement a lot of B-vitamins (including choline) without it.

- Nutritional and Acquired Deficiencies in Inositol Bioavailability. Correlations with Metabolic Disorders

"Inositol deficiency registered some interest during recent decades, mostly in an attempt to explain the therapeutic mechanism of lithium, credited to act by inducing a depletion of cellular inositol [65].

However, inositol deficiency may arise through a plethora of different mechanisms—including reduced food-dependent intake, increased catabolism, and excretion, decreased biosynthesis, inhibition of intestinal and cellular uptake—and can significantly affect several human pathological conditions [66]. In addition, despite myo-Ins deficiency being ascertained in different animal species [67], requirements for dietary inositol in man have still not been explicitly assessed. In addition, reliable estimation can be difficult because dietary necessities may be higher depending on the person’s age, the long-term use of antibiotics, or the regular consumption of a high amount of coffee [68] or other unknown diet components."

"Living organisms—from yeast to mammals—can synthetize myo-Ins up to 4–5 g/daily. This estimation indicates that the overall myo-Ins daily requirement in basal conditions (including both external sources and endogenous synthesis), should not be below the threshold value of 5–6 g. Yet, as the biosynthetic capability hugely varies among different tissues and independent of changing functional requirements (morphogenesis, sperm production, etc.), it can be hypothesized that myo-Ins biosynthesis should change accordingly."

"Cellular inositol uptake is [] decreased in the presence of high or even normal glucose concentrations. Namely, hyperglycemia induces myo-Ins depletion in nervous tissues, via competitive inhibition of sodium-dependent myo-Ins uptake [107]. By considering the structural similarities between myo-Ins and glucose, this result is far from surprising."

"Glucose may also induce myo-Ins depletion even through a biochemical pathway switching. Indeed, in diabetic patients, inositol depletion could arise due to the activation of the polyol pathway (glucose-sorbitol pathway), whereby glucose is first converted to sorbitol by aldose reductase and then to fructose by sorbitol dehydrogenase [110]." "Increased conversion of glucose into sorbitol significantly raises the intracellular osmolarity. To counteract that harmful event, cells actively inhibit the uptake of other relevant osmolytes (like inositol) and favor their cytosolic depletion, by downregulating the expression of specific carriers at the transcriptional level [112]."

"Increase in extracellular glucose (within the range mimicking the one observed in diabetes) caused marked decrease in the synthesis of phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol [115], resulting in chronic elevation of diacylglycerol (DAG), the chief physiological activator of protein kinase C (PKC) [116]. Moreover, the activation of the polyol pathway and the concomitantly reduction in cellular myo-Ins content can promote the oxidation of the NADPH/NADP+ and reduces the NADH/NAD+ redox couples, thereby perturbing a range of other adenine nucleotide-linked reactions. In diabetes, oxidation of NADPH/NADP+ may enhance susceptibility to oxidative tissue damage through depletion of reduced glutathione [117].

These findings not only provide further support to the hypothesis for which peripheral nerve integrity is highly dependent on the inositol-pathways [118], but also strengthen the link between hyperglycemia and deregulated inositol metabolism."

"Glucose-dependent depletion of cellular inositol storage has received further confirmation by a compelling body of observations. Hyperglycemia has been associated with an intracellular myo-inositol depletion in some tissues, especially in those susceptible of developing diabetes complications [119]. Moreover, hyperglycemia and insulin-resistance modify the relative proportion—namely by modulating the myo-Ins/d-chiro-Ins ratio—in which different inositol isomers are represented in different tissues [120]. In experimentally induced diabetes, inositol depletion—resulting from both cellular depletion and increased inositol urinary excretion—is an early marker of hyperglycemia and insulin resistance [102].

Myo-inositol depletion, in turn, may worsen insulin resistance and diabetes complication, including disturbances in cellular redox and free radical defense, increased oxidative glycation stress [121,122], and renal function. Conversely, myo-Ins supplementation improves several diabetes symptoms, as well as metabolic markers in a wide range of pathological conditions [123,124]."

"Inositol is chiefly catabolized in the kidney, where the enzyme myo-inositol oxygenase (MIOX) specifically metabolizes myo-Ins through the glucuronate-xylulose pathway." "Nephrectomy in animals impairs myo-Ins degradation, while renal failure is associated with significant abnormalities in myo-Ins metabolism and both inositol plasma and urinary levels [127]."

"Previous studies on animal models of diabetes documented an increased urinary loss involving only one isomer (myo-Ins or d-Chiro-Ins) [129,130], or both [128]. Similarly, in humans, increased urinary myo-inositol has been consistently demonstrated in both type 2 diabetes [120,131,132], and type 1 diabetes [133]."

"These findings suggest that deregulation of glucose metabolism will trigger abnormalities in myo-Ins metabolism and can increase the production of inositol-dependent toxic metabolites, which ultimately will damage renal function and promote inositol urinary loss. Therefore, it is likely that during hyperglycemia, insulin resistance and/or hypertension, changes in kidney metabolism are directly responsible for increased inositol loss, including both myo-Ins and d-Chiro-Ins isomers."​

- Inositol phospholipids in membrane function

--

What form of choline would you recommend? And thanks for all of the insight, by the way!

 

[Blossom]

Reduction in triglycerides and ldl cholesterol

Increased circulating E2

It seems like the lion's share of research regarding myo and d-chiro inositol is done on women with PCOS or with ovulation failure, so it's difficult to say if it's really beneficial for everyone else. It seems to improve insulin sensitivity and lower testosterone in women with PCOS, but these women are supposedly "hyperandrogenic." So it maybe that it is balancing out the excess for them, but in other people it might have other effects.

@freyasam I thought this post might interest you.

 

[freyasam]

@freyasam I thought this post might interest you.

Thanks for that, Blossom! I'm kind of brain foggy right now so I'm not sure if you're suggesting I look into inositol. If so, I tried it this year. It was amazing the first two weeks but then it made me depressed and more fatigued. :/ I wish it had kept working.

 

[Blossom]

Thanks for that, Blossom! I'm kind of brain foggy right now so I'm not sure if you're suggesting I look into inositol. If so, I tried it this year. It was amazing the first two weeks but then it made me depressed and more fatigued. :/ I wish it had kept working.

Yes, I read your thread on the ovarian and insulin resistance issue and thought of you when I saw this post but I wasn’t sure if you’d tried it before.

 

[lollipop]

Some would say this is the best way to get your inositol: IP6 Research

Hi @Dave Clark, I noticed you have mentioned this product on several threads. Do you take it? For how long? How much per day? Main benefits you noticed? Any side effects you noticed?

Than you for your time in answering these questions, I am curious...

 

[Zpol]

Yeah inositol pure powder actually tastes amazing. How much do you dose?

I take 2g myo-inositol plus 50 mg D-chiro 2x per day.

 

[Amazoniac]

What form of choline would you recommend? And thanks for all of the insight, by the way!

As you know, it's safer to get it from foods. But if you need to supplement and can afford using Zeus' Mitolipin* as a choline supplement, it's the best option that I'm aware. It provides about 28 mg or so per serving, so a bottle will be used quite fast.
If only saturated lecithin was available.. it provides a mixture of the phospholipids (including inositol).

*Cardiolipin should be renamed to mitolipin.

 

[Dave Clark]

Hi @Dave Clark, I noticed you have mentioned this product on several threads. Do you take it? For how long? How much per day? Main benefits you noticed? Any side effects you noticed?

Than you for your time in answering these questions, I am curious...

I found Dr. Shamsuddin's research compelling. I don't think there are too many ways to keep iron levels down as we age, and IP-6 seems to do a good job without having to do phlebotomy. Ray isn't a fan of phytates, and I agree they may be an issue with food, but the recommended way to use an IP-6/inositol supplement is to take it away from food on an empty stomach. Ray is also not a fan of iron, since it is a free radical catalyst. So, as Dr. Shamsuddin has recommended (and he has been using it for 18 years), take two capsules/twice per day on an empty stomach. I have been using the IP-6 Gold (they sent me their COA) as it seems to be a pure product. I also 'pulse dose' it, meaning 5 days on, two days off, I do this for several different nutrients since I think it is good to cycle things (on the off days I use LEF's lactoferrin product). I have not noticed any negative issues with using it, no tiredness or anything. I can't really feel anything tangible on the positive side either, but I have only been on it for a few months. I have read that IP-6 can help with copper zinc balance as well, probably by controlling the iron, not sure, I can't find a lot of research on that issue. I will post anything positive or negative that I experience.

 

[lollipop]

I found Dr. Shamsuddin's research compelling. I don't think there are too many ways to keep iron levels down as we age, and IP-6 seems to do a good job without having to do phlebotomy. Ray isn't a fan of phytates, and I agree they may be an issue with food, but the recommended way to use an IP-6/inositol supplement is to take it away from food on an empty stomach. Ray is also not a fan of iron, since it is a free radical catalyst. So, as Dr. Shamsuddin has recommended (and he has been using it for 18 years), take two capsules/twice per day on an empty stomach. I have been using the IP-6 Gold (they sent me their COA) as it seems to be a pure product. I also 'pulse dose' it, meaning 5 days on, two days off, I do this for several different nutrients since I think it is good to cycle things (on the off days I use LEF's lactoferrin product). I have not noticed any negative issues with using it, no tiredness or anything. I can't really feel anything tangible on the positive side either, but I have only been on it for a few months. I have read that IP-6 can help with copper zinc balance as well, probably by controlling the iron, not sure, I can't find a lot of research on that issue. I will post anything positive or negative that I experience.

Thank you so much for taking the time. Definitely post back as it sounds interesting. The research seems fairly solid.

 

[alywest]

As you know, it's safer to get it from foods. But if you need to supplement and can afford using Zeus' Mitolipin* as a choline supplement, it's the best option that I'm aware. It provides about 28 mg or so per serving, so a bottle will be used quite fast.
If only saturated lecithin was available.. it provides a mixture of the phospholipids (including inositol).

*Cardiolipin should be renamed to mitolipin.

Incorporation of acetate into fatty acids and lecithin by lung slices from fetal and newborn lambs
"The adult lung is also capable of incorporating glucose, palmitic acid, and linoleic acid into phospholipids (10, 13) and specifically into lecithin (14, 15)."

Would Zeus' DeFibron perhaps be useful in producing saturated lecithin endogenously?

"Although phosphatidyl ethanolamine may not be a major precursor of lecithin (34, 35), except in the liver, it is believed to be converted to lecithin by transmethylation in that organ (36, 37). Our results suggest that the amount of lecithin converted from phosphatidyl ethanolamine in the lung may be much smaller than that from other pathways, such as through the reaction of D-a,@-diglyceride with CDPcholine (38, 39) or acylation of lysolecithin (40-42). "

I think I am going to have to get MitoLipin in my next round of idealabs purchases.

 

[Amazoniac]

Incorporation of acetate into fatty acids and lecithin by lung slices from fetal and newborn lambs
"The adult lung is also capable of incorporating glucose, palmitic acid, and linoleic acid into phospholipids (10, 13) and specifically into lecithin (14, 15)."

Would Zeus' DeFibron perhaps be useful in producing saturated lecithin endogenously?

"Although phosphatidyl ethanolamine may not be a major precursor of lecithin (34, 35), except in the liver, it is believed to be converted to lecithin by transmethylation in that organ (36, 37). Our results suggest that the amount of lecithin converted from phosphatidyl ethanolamine in the lung may be much smaller than that from other pathways, such as through the reaction of D-a,@-diglyceride with CDPcholine (38, 39) or acylation of lysolecithin (40-42). "

I think I am going to have to get MitoLipin in my next round of idealabs purchases.

As far as I know they're not the limiting nutrients. If the body is having trouble synthesizing choline or inositol (which is what the previous post is about) for example, you can have plenty of those fats around but they won't be used for such purpose. It's also a more elaborated process when they're not provided already as phospholipids, the body tends break everything down to reassemble (Terma, 2018) and with that some might not be used for cell structure.

 

[alywest]

As far as I know they're not the limiting nutrients. If the body is having trouble synthesizing choline or inositol (which is what the previous post is about) for example, you can have plenty of those fats around but they won't be used for such purpose. It's also a more elaborated process when they're not provided already as phospholipids, the body tends break everything down to reassemble (Terma, 2018) and with that some might not be used for cell structure.

OK thanks

 

[Amazoniac]

Worth reading and checking out references 40-46:

- Iodine and Myo-Inositol: A Novel Promising Combination for Iodine Deficiency

"Interestingly, myo-inositol helps thyroid-hormone-producing cells to become more efficient and faster at building T4 (32, 41). This might be ascribable to a higher availability of iodine, whose organification is boosted by myo-inositol action. Indeed, myo-inositol is involved in one of the first steps of thyroid hormone production and modulates the H2O2-mediated iodination through the phospholipase C-dependent inositol phosphate Ca2+/diacylglycerol pathway, resulting in increased H2O2 generation (Figure 1). Differently, the cAMP cascade, induced by the TSH activity (through the TSH receptor activation), is more involved in cell growth and differentiation, and in thyroid hormones secretion. As myo-inositol plays a crucial role in the regulation of iodine organification, supplementation may promote faster recovery from ID. Indeed, H2O2 generated under the stimulus of myo-inositol is available for iodine incorporation inside the thyroid (33, 48). Such activity makes myo-inositol very appealing as a novel molecule to increase iodine availability."​

 

[Homo Consumericus]

What form of choline would you recommend? And thanks for all of the insight, by the way!

Eggs

 

[Homo Consumericus]

Worth reading and checking out references 40-46:

- Iodine and Myo-Inositol: A Novel Promising Combination for Iodine Deficiency

"Interestingly, myo-inositol helps thyroid-hormone-producing cells to become more efficient and faster at building T4 (32, 41). This might be ascribable to a higher availability of iodine, whose organification is boosted by myo-inositol action. Indeed, myo-inositol is involved in one of the first steps of thyroid hormone production and modulates the H2O2-mediated iodination through the phospholipase C-dependent inositol phosphate Ca2+/diacylglycerol pathway, resulting in increased H2O2 generation (Figure 1). Differently, the cAMP cascade, induced by the TSH activity (through the TSH receptor activation), is more involved in cell growth and differentiation, and in thyroid hormones secretion. As myo-inositol plays a crucial role in the regulation of iodine organification, supplementation may promote faster recovery from ID. Indeed, H2O2 generated under the stimulus of myo-inositol is available for iodine incorporation inside the thyroid (33, 48). Such activity makes myo-inositol very appealing as a novel molecule to increase iodine availability."​

Thanks for sharing.