What to do about male pattern baldness?

[Lee Simeon]

What to do about thin hair and male pattern baldness? Has anybody noticed any effects from taking any supplement? Already have good Vitamin D status.

 

[Hans]

There are so many aspects to cover:
- Avoid gut-irritating foods
- Balance blood sugar
- Avoid hyperinsulinemia (can be checked via c-peptide)
- Get all your macros
- Get all your micros
- Destress and minimize life stressors as much as possible
- Sleep enough
- Avoid environmental toxins (shampoo, shaving cream, deodorant, lotions, plastics, drugs, tap water, air pollution, mold, etc, etc)
- Get sunlight frequently on your head
- Do earthing/grounding
- Keep homocysteine low and improve blood flow
- Optimize cellular function and ATP production
- etc.

You can always try topical progesterone, Cardenosine, Solban and red light to improve cellular function. Also perhaps topical TyroMix on the scalp.

 

[Motif]

There are so many aspects to cover:

- Avoid gut-irritating foods
- Balance blood sugar
- Avoid hyperinsulinemia (can be checked via c-peptide)
- Get all your macros
- Get all your micros
- Destress and minimize life stressors as much as possible
- Sleep enough
- Avoid environmental toxins (shampoo, shaving cream, deodorant, lotions, plastics, drugs, tap water, air pollution, mold, etc, etc)
- Get sunlight frequently on your head
- Do earthing/grounding
- Keep homocysteine low and improve blood flow
- Optimize cellular function and ATP production
- etc.

You can always try topical progesterone, Cardenosine, Solban and red light to improve cellular function. Also perhaps topical TyroMix on the scalp.

What would a good diet look like in your opinion?

 

[johnwester130]

What to do about thin hair and male pattern baldness? Has anybody noticed any effects from taking any supplement? Already have good Vitamin D status.

Inflammation and fibrosis of the scalp cause baldness

Topical Pirfenidone - The real answer to inflammation and fibrosis. Not taurine, MSM, serrapeptase etc

A google search for antifibrotic drugs shows nintedanib (Ofev®) and pirfenidone Interestingly this was picked up on hairlosstalk too also called KitosCell Gel, probably easier to find. It works topically, many people use it on scars...

raypeatforum.com

 

[Hans]

There are so many aspects to cover:

What would a good diet look like in your opinion?

Meat, eggs, A2 milk, fruit and starches that you tolerate.

 

[Motif]

Meat, eggs, A2 milk, fruit and starches that you tolerate.

Is goat milk good?
Any advice for people who can’t eat that much , only thing I can eat a lot of is mashy stuff or yogurt / pudding stuff

 

[Hans]

Is goat milk good?

Yes definitely.

Any advice for people who can’t eat that much , only thing I can eat a lot of is mashy stuff or yogurt / pudding stuff

Smoothies with milk or yogurt and collagen, fruit and eggs are good. High fat foods can also quickly increase calories.

 

[lampofred]

It seems to me like MPB (and aging in general) is caused by blowing off more CO2 than you are producing, which leads to rise of stress hormones like estrogen, PTH, TSH, etc. Coffee, aspirin, calcium, salt, vitamin D, PUFA avoidance, thyroid, etc. help to raise CO2. I think the main things that lower CO2 are PUFA and phosphate.

 

[Motif]

It seems to me like MPB (and aging in general) is caused by blowing off more CO2 than you are producing, which leads to rise of stress hormones like estrogen, PTH, TSH, etc. Coffee, aspirin, calcium, salt, vitamin D, PUFA avoidance, thyroid, etc. help to raise CO2. I think the main things that lower CO2 are PUFA and phosphate.

Whatelse would help ?

Yes definitely.

Smoothies with milk or yogurt and collagen, fruit and eggs are good. High fat foods can also quickly increase calories.

thx!

 

[Vins7]

There are so many aspects to cover:
- Avoid gut-irritating foods
- Balance blood sugar
- Avoid hyperinsulinemia (can be checked via c-peptide)
- Get all your macros
- Get all your micros
- Destress and minimize life stressors as much as possible
- Sleep enough
- Avoid environmental toxins (shampoo, shaving cream, deodorant, lotions, plastics, drugs, tap water, air pollution, mold, etc, etc)
- Get sunlight frequently on your head
- Do earthing/grounding
- Keep homocysteine low and improve blood flow
- Optimize cellular function and ATP production
- etc.

You can always try topical progesterone, Cardenosine, Solban and red light to improve cellular function. Also perhaps topical TyroMix on the scalp.

Not using shampoo?

 

[Vins7]

It seems to me like MPB (and aging in general) is caused by blowing off more CO2 than you are producing, which leads to rise of stress hormones like estrogen, PTH, TSH, etc. Coffee, aspirin, calcium, salt, vitamin D, PUFA avoidance, thyroid, etc. help to raise CO2. I think the main things that lower CO2 are PUFA and phosphate.

Main source of phosphate is meat?

 

[OccamzRazer]

What to do about thin hair and male pattern baldness? Has anybody noticed any effects from taking any supplement? Already have good Vitamin D status.

Sexual transmutation exercises

Yoga/functional movements

Raw milk if tolerated

Dermastamping with niacinamide solution

 

[lampofred]

Main source of phosphate is meat?

Meat is a major source of phosphate, but I also think it might be important to focus on the ratio between fat and sugar rather than absolute phosphate intake (as long as you're still getting a generous amount of calcium in the diet). A low fat, high carb diet would likely raise metabolism enough to detox any phosphate you intake through a moderate amount of meat (so that meat intake doesn't have to be 0), whereas a high fat, low carb diet would probably cause even small amounts of phosphate to accumulate.

 

[lampofred]

Whatelse would help ?

By "etc." I just meant all the things the Peat usually recommends. A non-diet thing would be to maintain focused attention. Focus (like the type of focus needed to be a good painter, or to solve difficult math problems) causes CO2 retention. I've noticed that people with ADHD tend to have more baldness than average. And diet-wise, orange juice, milk, cheese, capsaicin, and white button mushrooms in particular raise it a lot. Also just keeping fat intake low in general (even saturated fat) would help.

 

[Motif]

By "etc." I just meant all the things the Peat usually recommends. A non-diet thing would be to maintain focused attention. Focus (like the type of focus needed to be a good painter, or to solve difficult math problems) causes CO2 retention. I've noticed that people with ADHD tend to have more baldness than average. And diet-wise, orange juice, milk, cheese, capsaicin, and white button mushrooms in particular raise it a lot. Also just keeping fat intake low in general (even saturated fat) would help.

That’s interesting. I have ADD too.

 

[Vins7]

Meat is a major source of phosphate, but I also think it might be important to focus on the ratio between fat and sugar rather than absolute phosphate intake (as long as you're still getting a generous amount of calcium in the diet). A low fat, high carb diet would likely raise metabolism enough to detox any phosphate you intake through a moderate amount of meat (so that meat intake doesn't have to be 0), whereas a high fat, low carb diet would probably cause even small amounts of phosphate to accumulate.

What ratio or macronutrient distribution do you think that is correct for being high carb/low fat?

 

[md_a]

I think that along with vitamin D / Sun , a diet that is based on a lot of potassium, calcium, magnesium, sodium should prevent and cure metabolic problems that include hair loss. In practice this means milk (raw), potato juice, fruit, vegetables, seafood, organ meats/ gelatin. Sufficient CO2 reflects the metabolic state.



„Magnesium and potassium are mainly intracellular ions, sodium and calcium are mainly extracellular ions. When cells are excited, stressed, or de-energized, they lose magnesium and potassium, and take up sodium and calcium. The mitochondria can bind a certain amount of calcium during stress, but accumulating calcium can reach a point at which it inactivates the mitochondria, forcing cells to increase their inefficient glycolytic energy production, producing an excess of lactic acid. Abnormal calcification begins in the mitochondria.

When cells are stressed or dying, they take up calcium, which tends to excite the cells at the same time that it inhibits their energy production, intensifying their stress. A cramp or a seizure is an example of uncontrolled cellular excitation. Prolonged excitation and stress contribute to tissue inflammation and fibrosis.

Gross calcification generally follows the fibrosis that is produced by inflammation.”Ray Peat



"One of the things that happen when there isn't enough sodium in the diet is that more aldosterone is synthesized. Aldosterone causes less sodium to be lost in the urine and sweat, but it achieves that at the expense of the increased loss of potassium, magnesium, and probably calcium. The loss of potassium leads to vasoconstriction, which contributes to heart and kidney failure and high blood pressure. The loss of magnesium contributes to vasoconstriction, inflammation, and bone loss. Magnesium deficiency is extremely common, but a little extra salt in the diet makes it easier to retain the magnesium in our foods."Ray Peat



.............

Taurine also interacts with sodium, potassium, and magnesium ions, leading to the containment of potassium and magnesium inside the cell and the prevention of excessive sodium and calcium entry.

............

Minoxidil exerts its action via opening of potassium channel,increases angiogenesis around the follicle by increasing the expressionof hair growth promoter such as vascular endothelial and hepatocyticgrowth factors.

Spironolactone is widely used in treatment of hypertension as analdosterone antagonist and a potassium sparing diuretic.

Error - Cookies Turned Off

..........

Androgenetic alopecia as an early marker for hypertension

Androgenetic alopecia as an early marker for hypertension El-Esawy FM, El-Rahman SH - Egypt J Dermatol Venerol

.......

Potassium inhibits dietary salt-induced transforming growth factor-beta production

Abstract

Human and animal studies demonstrate an untoward effect of excess dietary NaCl (salt) intake on cardiovascular function and life span. The endothelium in particular augments the production of transforming growth factor (TGF)-beta, a fibrogenic growth factor, in response to excess dietary salt intake. This study explored the initiating mechanism that regulates salt-induced endothelial cell production of TGF-beta. Male Sprague-Dawley rats were given diets containing different amounts of NaCl and potassium for 4 days. A bioassay for TGF-beta demonstrated increased (35.2%) amounts of active TGF-beta in the medium of aortic ring segments from rats on the high-salt diet compared with rats maintained on a 0.3% NaCl diet. Inhibition of the large-conductance, calcium-activated potassium channel inhibited dietary salt-induced vascular production of TGF-beta but did not affect production of TGF-beta by ring segments from rats on the low-salt diet. Immunohistochemical and Western analyses demonstrated the alpha subunit of the calcium-activated potassium channel in endothelial cells. Increasing medium [K+] inhibited production of dietary salt-induced vascular production levels of total and active TGF-beta but did not alter TGF-beta production by aortic rings from rats on the 0.3% NaCl diet. Increasing dietary potassium content decreased urinary active TGF-beta in animals receiving the high-salt diet but did not change urinary active TGF-beta in animals receiving the low-salt diet. The findings demonstrated an interesting interaction between the dietary intake of potassium and excess NaCl and further showed the fundamental role of the endothelial calcium-activated potassium channel in the vascular response to excess salt intake.

Potassium inhibits dietary salt-induced transforming growth factor-beta production - PubMed

.........

Effect of dietary salt on regulation of TGF-β in the kidney

Abstract

Dietary sodium chloride (salt) has long been considered injurious to the kidney by promoting the development of glomerular and tubulointerstitial fibrosis. Endothelial cells throughout the vasculature and glomeruli respond to increased dietary salt intake with increased production of transforming growth factor-β (TGF-β) and nitric oxide. High-salt intake activates large-conductance, voltage- and calcium-activated potassium (BK(Ca)) channels in endothelial cells. Activation of BK(Ca) channels promotes signaling through proline-rich tyrosine kinase-2, cellular-sarcoma (c-Src), Akt (also known as protein kinase B), and mitogen-activated protein kinase pathways that lead to endothelial production of TGF-β and nitric oxide. TGF-β signaling is broadly accepted as a strong stimulator of renal fibrosis. The classic description of TGF-β signaling pathology in renal disease involves signaling through Smad proteins resulting in extracellular matrix deposition and fibrosis. Active TGF-β1 also causes fibrosis by inducing epithelial-mesenchymal transition and apoptosis. By enhancing TGF-β signaling, increased dietary salt intake leads to progressive renal failure from nephron loss and glomerular and tubulointerstitial fibrosis.

Effect of dietary salt on regulation of TGF-β in the kidney - PubMed

.........

Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7

The proposed underlying mechanisms of the deleterious effect of potassium depletion include activation of the local renin-angiotensin II system (RAS) (32), increased angiotensin II receptor (AT1) expression (12), and altered activity of the sodium-potassium pump in the renal tubule (35), acting by blood pressure-dependent and/or blood pressure-independent mechanisms.

We examined the influence of potassium supplementation on the degree of renal inflammation in the subtotal nephrectomy model of CKD in rats. Our results indicate that potassium supplementation can reduce inflammatory processes in the kidney, and the degree of renal injury.

Renal expression of TGF-β and Smad7.

Because TGF-β and Smad7 play a critical role in the pathogenesis of progressive kidney injury, we examined the levels of TGF-β and Smad7 in the remnant kidney. We found that potassium supplementation significantly increased renal Smad7 expression compared with levels in the remnant kidneys from the basal diet. In contrast, potassium supplementation decreased renal TGF-β expression (Fig. 8, A and B).

DISCUSSION

Our results in a standard rat model of CKD demonstrate that potassium can play an important role in modulating renal inflammation. Specifically, we found that potassium supplementation 1) decreased the degree of interstitial histological injury and 2) suppressed renal inflammation as evidenced by decreased macrophage infiltration, lower expression of inflammatory cytokines, and decreased NF-κB activation. We postulate that the renoprotective mechanisms could be decreased renal TGF-β expression, upregulated renal Smad7 expression, and a reduction of blood pressure.



NF-κB plays a crucial role in mediating inflammation in the kidney because NF-κB regulates the expression of numerous genes involved in inflammation, including cytokines and adhesion molecules. In the resting state, cellular NF-κB dimers remain in the cytoplasm bound to the inhibitory subunit IκBα, which renders NF-κB inactive. Activation of NF-κB occurs when IκBα is phosphorylated in response to a number of stimuli, leading to IκBα ubiquitinylation and, ultimately, degradation by the proteasome. Therefore, NF-κB is released into the nucleus and regulates the transcription of target genes (2). Extensive in vitro studies in renal mesangial and tubular epithelial cells have demonstrated that NF-κB activation leads to upregulation of inflammatory gene expression (10, 14, 23, 26, 28, 33). Blockade of the NF-κB pathway can alleviate inflammatory reactions (5, 8, 22, 25, 37). In short, NF-κB plays a central role in mechanisms causing renal inflammation. In this study, we found that potassium supplementation decreased NF-κB activation even though there was no change in serum potassium concentration. Our results also show that the suppression of NF-κB activation is accompanied by upregulation of Smad7, an inhibitory Smad in the TGF-β/Smad signaling pathway, in the remnant kidney. This is relevant because Smad7 can function as an inhibitor of the inflammatory NF-κB signaling pathway as well as an inhibitor of the fibrotic TGF-β/Smad signaling pathway (21, 44). Our previous studies demonstrated that Smad7 plays an important role in the regulation of renal inflammation and fibrosis. For example, overexpression of Smad7 in the kidney inhibited renal fibrosis through a mechanism that not only involves inhibition of receptor-Smads activation but also an upregulation of IκBα to suppress NF-κB activation and inflammation (21, 44).



We also found that potassium supplementation decreased TGF-β expression in the remnant kidneys. There are extensive in vitro studies demonstrating that TGF-β can upregulate Smad7 expression (24). However, in animal studies the association between TGF-β and Smad7 expression has been inconsistent. For example, Uchida et al. (42) and Fukasawa et al. (13) reported that renal I-Smads Smad6/Smad7 were decreased in rat anti-Thy1 model and mouse UUO models, despite dramatic upregulation of TGF-β expression in the kidney. In agreement with aforementioned reports, we have found that a mouse unilateral uretheral obstructive model had a discrepancy between renal TGF-β and Smad7 expression levels. We do not know why the in vivo results differ from in vitro findings, but our results indicate that the renoprotective effect of potassium supplementation is associated with upregulation of Smad7 and downregulation of TGF-β in the remnant kidney.



High blood pressure is an important mediator in the progressive nature of CKD. In this study, the results show that potassium supplementation did not lead to substantial hyperkalemia, suggesting that part of supplementary potassium is replete in the intracellular potassium pool. Our results also show that potassium supplementation lowered blood pressure in this model of CKD, even though serum potassium level was almost unchanged, and this effect was independent of dietary protein, calories, sodium, or other nutrients because the rats were pair fed (Fig. 1). There are reports suggesting that high dietary potassium exerts a natriuretic and diuretic effect that could contribute to the lowering of blood pressure (27, 36). But we found no difference in urinary sodium excretion between CKD groups. We then assessed whether the production of aldosterone or angiotensin II contributed to the antihypertension effect of a high-potassium diet, and our further study showed that a high-potassium diet lowers blood pressure in this CKD model by a manner independent on aldosterone and angiotensin II production, because no significant difference was found in urine aldosterone/angiotensin II excretion (Fig. 2, D and E). We have not identified how dietary potassium supplementation lowers blood pressure. Possible explanations include a dilatation of blood vessels. For example, our previous study suggested that a high-potassium diet vasodilates vessels by stimulating the activity of Na+-K+-ATPase to decrease cytosolic Ca2+ concentration (9). A high-potassium diet might also enhance endothelium-dependent relaxation and increase nitric oxide synthesis to dilate blood vessels (48). Regardless of the mechanism, the blood pressure-lowering effect of dietary potassium was only moderate but could be very important, since there are beneficial effects on local tissue/organ structure and function in some interventional studies (15, 18, 43).



In summary, we have demonstrated that potassium supplementation in amounts that do not lead to severe hyperkalemia exert a renoprotective effect in a standard rat CKD model. Upregulation of Smad7 expression in the kidney and inhibition of NF-κB activation are suggested mechanisms for the renoprotective effect against renal inflammation. The antihypertensive effects of potassium as well as downregulation of renal TGF-β expression could also contribute to renoprotection. These results suggested that careful modification of dietary potassium intake maybe important in the management of CKD.

Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7 | American Journal of Physiology-Renal Physiology

 

[Motif]

I think that along with vitamin D / Sun , a diet that is based on a lot of potassium, calcium, magnesium, sodium should prevent and cure metabolic problems that include hair loss. In practice this means milk (raw), potato juice, fruit, vegetables, seafood, organ meats/ gelatin. Sufficient CO2 reflects the metabolic state.



„Magnesium and potassium are mainly intracellular ions, sodium and calcium are mainly extracellular ions. When cells are excited, stressed, or de-energized, they lose magnesium and potassium, and take up sodium and calcium. The mitochondria can bind a certain amount of calcium during stress, but accumulating calcium can reach a point at which it inactivates the mitochondria, forcing cells to increase their inefficient glycolytic energy production, producing an excess of lactic acid. Abnormal calcification begins in the mitochondria.

When cells are stressed or dying, they take up calcium, which tends to excite the cells at the same time that it inhibits their energy production, intensifying their stress. A cramp or a seizure is an example of uncontrolled cellular excitation. Prolonged excitation and stress contribute to tissue inflammation and fibrosis.

Gross calcification generally follows the fibrosis that is produced by inflammation.”Ray Peat



"One of the things that happen when there isn't enough sodium in the diet is that more aldosterone is synthesized. Aldosterone causes less sodium to be lost in the urine and sweat, but it achieves that at the expense of the increased loss of potassium, magnesium, and probably calcium. The loss of potassium leads to vasoconstriction, which contributes to heart and kidney failure and high blood pressure. The loss of magnesium contributes to vasoconstriction, inflammation, and bone loss. Magnesium deficiency is extremely common, but a little extra salt in the diet makes it easier to retain the magnesium in our foods."Ray Peat



.............

Taurine also interacts with sodium, potassium, and magnesium ions, leading to the containment of potassium and magnesium inside the cell and the prevention of excessive sodium and calcium entry.

............

Minoxidil exerts its action via opening of potassium channel,increases angiogenesis around the follicle by increasing the expressionof hair growth promoter such as vascular endothelial and hepatocyticgrowth factors.

Spironolactone is widely used in treatment of hypertension as analdosterone antagonist and a potassium sparing diuretic.

Error - Cookies Turned Off

..........

Androgenetic alopecia as an early marker for hypertension

Androgenetic alopecia as an early marker for hypertension El-Esawy FM, El-Rahman SH - Egypt J Dermatol Venerol

.......

Potassium inhibits dietary salt-induced transforming growth factor-beta production

Abstract

Human and animal studies demonstrate an untoward effect of excess dietary NaCl (salt) intake on cardiovascular function and life span. The endothelium in particular augments the production of transforming growth factor (TGF)-beta, a fibrogenic growth factor, in response to excess dietary salt intake. This study explored the initiating mechanism that regulates salt-induced endothelial cell production of TGF-beta. Male Sprague-Dawley rats were given diets containing different amounts of NaCl and potassium for 4 days. A bioassay for TGF-beta demonstrated increased (35.2%) amounts of active TGF-beta in the medium of aortic ring segments from rats on the high-salt diet compared with rats maintained on a 0.3% NaCl diet. Inhibition of the large-conductance, calcium-activated potassium channel inhibited dietary salt-induced vascular production of TGF-beta but did not affect production of TGF-beta by ring segments from rats on the low-salt diet. Immunohistochemical and Western analyses demonstrated the alpha subunit of the calcium-activated potassium channel in endothelial cells. Increasing medium [K+] inhibited production of dietary salt-induced vascular production levels of total and active TGF-beta but did not alter TGF-beta production by aortic rings from rats on the 0.3% NaCl diet. Increasing dietary potassium content decreased urinary active TGF-beta in animals receiving the high-salt diet but did not change urinary active TGF-beta in animals receiving the low-salt diet. The findings demonstrated an interesting interaction between the dietary intake of potassium and excess NaCl and further showed the fundamental role of the endothelial calcium-activated potassium channel in the vascular response to excess salt intake.

Potassium inhibits dietary salt-induced transforming growth factor-beta production - PubMed

.........

Effect of dietary salt on regulation of TGF-β in the kidney

Abstract

Dietary sodium chloride (salt) has long been considered injurious to the kidney by promoting the development of glomerular and tubulointerstitial fibrosis. Endothelial cells throughout the vasculature and glomeruli respond to increased dietary salt intake with increased production of transforming growth factor-β (TGF-β) and nitric oxide. High-salt intake activates large-conductance, voltage- and calcium-activated potassium (BK(Ca)) channels in endothelial cells. Activation of BK(Ca) channels promotes signaling through proline-rich tyrosine kinase-2, cellular-sarcoma (c-Src), Akt (also known as protein kinase B), and mitogen-activated protein kinase pathways that lead to endothelial production of TGF-β and nitric oxide. TGF-β signaling is broadly accepted as a strong stimulator of renal fibrosis. The classic description of TGF-β signaling pathology in renal disease involves signaling through Smad proteins resulting in extracellular matrix deposition and fibrosis. Active TGF-β1 also causes fibrosis by inducing epithelial-mesenchymal transition and apoptosis. By enhancing TGF-β signaling, increased dietary salt intake leads to progressive renal failure from nephron loss and glomerular and tubulointerstitial fibrosis.

Effect of dietary salt on regulation of TGF-β in the kidney - PubMed

.........

Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7

The proposed underlying mechanisms of the deleterious effect of potassium depletion include activation of the local renin-angiotensin II system (RAS) (32), increased angiotensin II receptor (AT1) expression (12), and altered activity of the sodium-potassium pump in the renal tubule (35), acting by blood pressure-dependent and/or blood pressure-independent mechanisms.

We examined the influence of potassium supplementation on the degree of renal inflammation in the subtotal nephrectomy model of CKD in rats. Our results indicate that potassium supplementation can reduce inflammatory processes in the kidney, and the degree of renal injury.

Renal expression of TGF-β and Smad7.

Because TGF-β and Smad7 play a critical role in the pathogenesis of progressive kidney injury, we examined the levels of TGF-β and Smad7 in the remnant kidney. We found that potassium supplementation significantly increased renal Smad7 expression compared with levels in the remnant kidneys from the basal diet. In contrast, potassium supplementation decreased renal TGF-β expression (Fig. 8, A and B).

DISCUSSION

Our results in a standard rat model of CKD demonstrate that potassium can play an important role in modulating renal inflammation. Specifically, we found that potassium supplementation 1) decreased the degree of interstitial histological injury and 2) suppressed renal inflammation as evidenced by decreased macrophage infiltration, lower expression of inflammatory cytokines, and decreased NF-κB activation. We postulate that the renoprotective mechanisms could be decreased renal TGF-β expression, upregulated renal Smad7 expression, and a reduction of blood pressure.



NF-κB plays a crucial role in mediating inflammation in the kidney because NF-κB regulates the expression of numerous genes involved in inflammation, including cytokines and adhesion molecules. In the resting state, cellular NF-κB dimers remain in the cytoplasm bound to the inhibitory subunit IκBα, which renders NF-κB inactive. Activation of NF-κB occurs when IκBα is phosphorylated in response to a number of stimuli, leading to IκBα ubiquitinylation and, ultimately, degradation by the proteasome. Therefore, NF-κB is released into the nucleus and regulates the transcription of target genes (2). Extensive in vitro studies in renal mesangial and tubular epithelial cells have demonstrated that NF-κB activation leads to upregulation of inflammatory gene expression (10, 14, 23, 26, 28, 33). Blockade of the NF-κB pathway can alleviate inflammatory reactions (5, 8, 22, 25, 37). In short, NF-κB plays a central role in mechanisms causing renal inflammation. In this study, we found that potassium supplementation decreased NF-κB activation even though there was no change in serum potassium concentration. Our results also show that the suppression of NF-κB activation is accompanied by upregulation of Smad7, an inhibitory Smad in the TGF-β/Smad signaling pathway, in the remnant kidney. This is relevant because Smad7 can function as an inhibitor of the inflammatory NF-κB signaling pathway as well as an inhibitor of the fibrotic TGF-β/Smad signaling pathway (21, 44). Our previous studies demonstrated that Smad7 plays an important role in the regulation of renal inflammation and fibrosis. For example, overexpression of Smad7 in the kidney inhibited renal fibrosis through a mechanism that not only involves inhibition of receptor-Smads activation but also an upregulation of IκBα to suppress NF-κB activation and inflammation (21, 44).



We also found that potassium supplementation decreased TGF-β expression in the remnant kidneys. There are extensive in vitro studies demonstrating that TGF-β can upregulate Smad7 expression (24). However, in animal studies the association between TGF-β and Smad7 expression has been inconsistent. For example, Uchida et al. (42) and Fukasawa et al. (13) reported that renal I-Smads Smad6/Smad7 were decreased in rat anti-Thy1 model and mouse UUO models, despite dramatic upregulation of TGF-β expression in the kidney. In agreement with aforementioned reports, we have found that a mouse unilateral uretheral obstructive model had a discrepancy between renal TGF-β and Smad7 expression levels. We do not know why the in vivo results differ from in vitro findings, but our results indicate that the renoprotective effect of potassium supplementation is associated with upregulation of Smad7 and downregulation of TGF-β in the remnant kidney.



High blood pressure is an important mediator in the progressive nature of CKD. In this study, the results show that potassium supplementation did not lead to substantial hyperkalemia, suggesting that part of supplementary potassium is replete in the intracellular potassium pool. Our results also show that potassium supplementation lowered blood pressure in this model of CKD, even though serum potassium level was almost unchanged, and this effect was independent of dietary protein, calories, sodium, or other nutrients because the rats were pair fed (Fig. 1). There are reports suggesting that high dietary potassium exerts a natriuretic and diuretic effect that could contribute to the lowering of blood pressure (27, 36). But we found no difference in urinary sodium excretion between CKD groups. We then assessed whether the production of aldosterone or angiotensin II contributed to the antihypertension effect of a high-potassium diet, and our further study showed that a high-potassium diet lowers blood pressure in this CKD model by a manner independent on aldosterone and angiotensin II production, because no significant difference was found in urine aldosterone/angiotensin II excretion (Fig. 2, D and E). We have not identified how dietary potassium supplementation lowers blood pressure. Possible explanations include a dilatation of blood vessels. For example, our previous study suggested that a high-potassium diet vasodilates vessels by stimulating the activity of Na+-K+-ATPase to decrease cytosolic Ca2+ concentration (9). A high-potassium diet might also enhance endothelium-dependent relaxation and increase nitric oxide synthesis to dilate blood vessels (48). Regardless of the mechanism, the blood pressure-lowering effect of dietary potassium was only moderate but could be very important, since there are beneficial effects on local tissue/organ structure and function in some interventional studies (15, 18, 43).



In summary, we have demonstrated that potassium supplementation in amounts that do not lead to severe hyperkalemia exert a renoprotective effect in a standard rat CKD model. Upregulation of Smad7 expression in the kidney and inhibition of NF-κB activation are suggested mechanisms for the renoprotective effect against renal inflammation. The antihypertensive effects of potassium as well as downregulation of renal TGF-β expression could also contribute to renoprotection. These results suggested that careful modification of dietary potassium intake maybe important in the management of CKD.

Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7 | American Journal of Physiology-Renal Physiology

I bet this is really important. Still I have no idea how to really balance it.

I feel like I could add two big spoons of salt daily, but i don’t know if it’s harmful or not.

 

[md_a]

I bet this is really important. Still I have no idea how to really balance it.

I feel like I could add two big spoons of salt daily, but i don’t know if it’s harmful or not.

I wanted to emphasize on my post that enough potassium is needed in addition to calcium, magnesium, sodium.

 

[Hans]

Not using shampoo?

I use Palmers brand which works really good and is pretty clean.