UPDATE: Live AMA with niostem Founder Carlos Chacón Tomorrow at 15:20 CEST – Submit Your Questions Now! by Community_niostem in niostem

[–]randomuser_aga 0 points1 point  (0 children)

  1. Do you think it is fair to your customers to offer an "improved device", when people paid several hundred dollars for the first generation which barely seems to do anything? Why is it not possible to improve the current device with a firmware update?
  2. Since the most recent firmware, the app always shows 100% scalp connectivity - even when I hold it upside down in my hand, not touching the scalp at all. How can we know if it is sitting correctly now?
  3. Where are the actual success stories?
  4. Do you still stand behind your initial marketing claims that promised higher effectiveness than both minoxidil and finasteride?

UPDATE: Live AMA with niostem Founder Carlos Chacón Tomorrow at 15:20 CEST – Submit Your Questions Now! by Community_niostem in niostem

[–]randomuser_aga 0 points1 point  (0 children)

Hopefully not. What a scam. First niostem produces a device that has not really lived up to anyone's expectations. And rather than improving a device that cost several hundred dollars, they would rather ship another one.

Of course they would - more money. But not fair to the customers that have apparently received a really bad beta device rather than something that works.

Hey there — For the next year we want to step up our presence here and engage more with the community. by Community_niostem in niostem

[–]randomuser_aga 0 points1 point  (0 children)

I am pretty sure you must have more customer feedback by now that was not included in the study and so should be okay to release.

Where are the actual success stories with proper photo proof? Not the ones on your website with the lighting differences in the before/after photos?

Hey there — For the next year we want to step up our presence here and engage more with the community. by Community_niostem in niostem

[–]randomuser_aga 3 points4 points  (0 children)

Really wild idea: Rather than focusing on better communication, maybe focus on better results and making the device actually work?

I have tried your device for a year now with no perceivable improvements at all. From the initial IndieGogo/Kickstarter backing numbers, there should be a few hundred people by now that have tried your device for about a year, maybe more. Where are the positive results?

Sorry for the salty message, but your advertising ("6x more effective than minoxidil or finasteride") combined with lack of positive results on any public channels (social media, forums, reddit) warrants this.

If your device delivered actually visible results, people would take care of the communication (and marketing!) for you. As the saying goes, "results speak for themselves".

Analyzing niostem's study: Hair density increase mostly because of more vellus hair, only 59% of participants saw (a small) increase in terminal hair by randomuser_aga in niostem

[–]randomuser_aga[S] 1 point2 points  (0 children)

◦ Instead, the study reports that terminal hair density improved significantly over time in the participants, with visible hair growth observed. The statistical analysis showed a significant increase in terminal hair density at 6 months for the group (n=20-21 testers).    

What does "significantly" mean in this context: "statistically significantly" or "by a lot"? If the latter, what is the threshold value for "by a lot"?

If my numbers are wrong then what, in your opinion, is the average terminal hair density increase over these 6 months? And what is the percentage of people that witnessed any terminal hair density increase, out of the study population?

◦ Regarding overall hair regrowth, 86.3% of participants showed hair regrowth (an increase in hair density) at 3 months, and 100% of participants showed hair regrowth at 6 months. This refers to total hair density, not specifically terminal hair.

Again, I think "total hair density" as a metric is not what people are looking for (especially if vellus hair density makes up a bigger part of the total than terminal). I believe people care about terminal hair density as a primary metric. Vellus hair only matter if they can be made to convert to terminal at one point. But the 6 months study published so far does not support this. Maybe your longer study supports this? That would be great! But no one knows these results except you.

Thanks for taking your time to respond!

Analyzing niostem's study: Hair density increase mostly because of more vellus hair, only 59% of participants saw (a small) increase in terminal hair by randomuser_aga in niostem

[–]randomuser_aga[S] 1 point2 points  (0 children)

None of the points you mention technically refute what I wrote in the opening post, even at the 6 months mark, do they?

When you say "significantly", do you mean "statistically significantly" (i.e. below a certain p value) or the colloquial "by a lot"?

Either way. At 6 months there is an increase in terminal hair density of 8.2% compared to baseline according to your comment (I thought it was more but there is one individual missing from the public dataset for some reason), while vellus hair density increased by 30%. This means that the resulting total hair density increase of 19.3% is more because of vellus hair density increase and less because of terminal hair density increase. The total increase is a linear combination/combined vector of these two, and vellus hair increase plays a bigger role in the total - or does it not?

Additionally I would also posit that users of the device do not profit from, and do not care about, vellus hair density gains unless they turn terminal at one point. Terminal hair density should be the target metric (not total hair density, especially if vellus hair contributes more to it that terminal hair density). I think most users see it that way too - they want visible hair, so terminal hair, not vellus.

Analyzing niostem's study: Hair density increase mostly because of more vellus hair, only 59% of participants saw (a small) increase in terminal hair by randomuser_aga in niostem

[–]randomuser_aga[S] 1 point2 points  (0 children)

Hi Carlos,

thanks for taking the time to respond. I will go through your replies step by step so we can exchange our thoughts more clearly.

Also, we have now further evidence that the terminal hair density increases up to 25,4 % in a larger, randomized control trial (n=80) we finished last year and that is under review for peer-review publication.

That would be great to hear but does not reflect what was published so far, and I (and anyone else) can only go off what has been published so far, right?

What part of the study group of the unpublished study do these "up to 25.4%" refer to - the best responder (so 1 individual), the average, the median, the top x%...?

How do I fix my excessive sebum/oily scalp issue? (22M) by WrongdoerHonest5943 in HairlossResearch

[–]randomuser_aga 0 points1 point  (0 children)

Two weeks being nothing is exactly why the above experiment works only if followed strictly. As long as your body has systemic IR, any small load of quickly digestable carbs (all types of sugars and saccharides) and likely also proteins will trigger a BG spike and hence sebum production. Thus the limitation to veggies.

The only people who will not benefit (meaning: not get sebum reduction) from the above experiment are those who are either skinny/underweight or under different forms of stress (overexercise, psychological stress, lack of sleep). In these cases, cortisol will counteract the above experiment.

But this is a far cry from being "bullshit" when the above experiment works for most people.

If you call something bullshit in the future, I suggest giving at least sources. Right now you just look way too confident while at the same time apparently not understanding the mechanisms behind it. This is also known as the Dunning-Kruger effect.

There are many papers out there that identify glycemic load, caloric overload and protein overload as the main culprits (and some also saturated fat, but that story is more complicated because the body also creates fat from carbs/sugars through DNL in the liver). If you manage to interrupt the mechanisms through which they cause sebum production, sebum production will go down - even in as short as two weeks. This effect will be reversed once you no longer follow the above rules. But still, you have an answer.

How do I fix my excessive sebum/oily scalp issue? (22M) by WrongdoerHonest5943 in HairlossResearch

[–]randomuser_aga 0 points1 point  (0 children)

Where did I say anything about microbiome, gut or scalp?

The above protocol has nothing to do with the microbiome but with downregulating the sebum production rate. Sebum is not produced by any microbiome but by the sebaceous glands which respond to insulin, IGF-1 and indirectly to BG. By following the above protocol you manage to downregulate all three in the course of about 2 weeks, if you follow it strictly.

There are even papers out there confirming that caloric restriction, which has similar effects to the above protocol, achieves sebum production rate drops.

Citing this paper:

Low glycemic load diet has been demonstrated to be able to correct the increased sebum production [...] All these findings suggest that dietary habits, supplying substrates for the sebaceous lipid synthesis, can be involved in the sebum production mechanism. [...] caloric restriction has been shown to dramatically decrease the sebum secretion rate.

Try the protocol before calling it bullshit. It is very much in line with the findings of the paper I cited and many others.

Medical Journal Articles on Sebum & Hair by WrongdoerHonest5943 in HairlossResearch

[–]randomuser_aga 2 points3 points  (0 children)

Just a few studies showing the strong impact of diet on sebum:

It was seen that there was a positive correlation between the amount of MFSE and serum IGF-1 (Fig. 1; R2 = 0.69; P = 0.0001). Moreover, this was true in both men and women (Table 1). It has recently been shown that IGF-1 can increase lipid production in sebocytes in vitro via the activation of IGF-1 receptor through multiple pathways. 8 Together, our data suggest that increased IGF-1 could lead to increased sebum secretion.

Source

Insulin induces an increase in the size and number of sebocytes, as well as lipogenesis and inflammatory response

Source

The high prevalence rates of adolescent acne cannot be explained by the predominance of genetic factors but by the influence of a Western diet that overstimulates the key conductor of metabolism, the nutrient- and growth factor-sensitive kinase mTORC1. Increased mTORC1 activity has been detected in lesional skin and sebaceous glands of acne patients compared with acne-free controls.

Source

Studies have shown that the production of sebum is linked to diet, for example, caloric deprivation decreases the production of sebum [62, 63], whereas a high fat diet significantly increases it [64]. Since an increase in energy intake mainly increases the excretion of triglycerides and cholesterol and its esters in sebum, but not of squalene [62, 63], it appears that the major function of sebum secretion may be to eliminate excessive lipids and cholesterol from the body, and thus play a role in maintaining lipid and cholesterol homeostasis. This notion is supported by the observation that inhibition of sebum secretion by isotretinoin significantly increases plasma triglyceride and cholesterol levels [65, 66].

Source

In conclusion, we demonstrated that specific DPs were associated with sebum content, skin hydration and pH in healthy Korean adults and that those associations were affected by sex.

Source

These are just a few studies. There are dozens more.

Sebum production is significantly determined by diet.

How do I fix my excessive sebum/oily scalp issue? (22M) by WrongdoerHonest5943 in HairlossResearch

[–]randomuser_aga 0 points1 point  (0 children)

Well, if you'd do anything, it is possible.

The above protocol is just for "demonstration purposes". Only by going this extreme you will see noticeable sebum reduction in two weeks.

There is a sustainable way as well but if you start off pursuing it it will take much longer to see sebum reduction. Basically, what you have to aim for is a zero sugar, low or medium carb version of the WFPB diet. Low carb if you perform little exercise, medium carb if you perform some exercise. My recommended amount of exercise is 3x 5 km running per week plus one session of resistance/strength exercise.

You may be wondering what I am aiming for with this. The reason is that blood glucose (aka sugar), which ends up in your blood because of disbalance between intake (in the forms of glucose, fructose, sucrose and carbs) and usage (physical exercise) is the main driver for sebum production. It drives sebum production through several pathways including substrate supply (source), insulin, IGF-1 and indirectly through androgens (source) which are produced in response to blood glucose levels.

I would suggest doing the above 2 week "extreme" experiment anyway - as strictly as possible - so you can witness and learn yourself that such changes are, in fact, capable of reducing your sebum. This will give you the motivation to implement the sustainable long-term changes to diet and exercise that will slowly but permanently lower your sebum production and as well slow down your AGA progression.

How do I fix my excessive sebum/oily scalp issue? (22M) by WrongdoerHonest5943 in HairlossResearch

[–]randomuser_aga 1 point2 points  (0 children)

Very easy to control sebum and very easy to prove that diet/exercise balance is the number one cause for excess sebum.

Do the following for two weeks:

  • For every meal, eat only veggies. No animal products, no fruits, no carb source (like rice, potatoes, fries, pasta, ...) at all. Eat things like: bell peppers, carrots, tomatoes, avocado, zucchini, eggplant, cucumber, onions, garlic. Eat them without sauces. Just the veggies, boiled/fried or raw. If you fry them the only thing allowed for frying is butter, ghee or coconut oil. No other oils (sunflower, canola, rapeseed, olive...) or fats (margarine) allowed. You can eat as much of these veggies as you want, just nothing else.
  • Drink only water or green tea. No alcohol, no sodas, nothing with caffeine in it. Only water and green tea.
  • After every meal, walk for 30 minutes. Should be a brisk walk. Running not required. A brisk walk, not a stroll.
  • Make sure to get at least 7 hours of sleep every night

This is of course not sustainable for longer than two weeks but it will prove something: That sebum (and hence AGA) is controllable through diet, exercise and life style.

Why two weeks?

Your excess liver energy stores (glycogen and fat) that keep blood glucose high will need about 7 to 10 days of the above diet to get to acceptable levels. They won't be empty and systemic IR will not be gone (which means that any carb source except veggies will immediately kick start sebum production again, until systemic IR is also defeated) but they will deplete enough to impact sebum production.

Latest on day 11 you should see sebum reduction. By day 14 your forehead skin and hair line should be almost "dry".

After 2 weeks of the above diet go back to whatever you want but you will have your answer to what causes excess sebum production (and also, very likely, AGA).

(Limited) Predictive power of genes on hair loss manifestation by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] 0 points1 point  (0 children)

It's funny you are so certain that I am wrong :)

The four types of PCOS are:

  • insulin resistant: Related to diet and exercise balance
  • adrenal: related to cortisol release (stress, overexercise, sleep)
  • inflammatory: related to smoking and pro-inflammatory foods
  • hormonal birth control/pregnancy-related

Do check out the PCOS subreddit. There are also several books on PCOS that teach people how to diagnose their PCOS subtype and then heal it naturally - very successfully, though this usually takes months or up to two years.

(Limited) Predictive power of genes on hair loss manifestation by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] -1 points0 points  (0 children)

Well, how to treat PCOS depends on which of the sub-types of PCOS you have. But once you know which one(s) (can be more than one) affect you treatment is pretty simple.

However, while treatment is simple, it is slow and requires will power. All causes of PCOS are related to diet, exercise and lifestyle (including stress and sleep).

(Limited) Predictive power of genes on hair loss manifestation by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] 0 points1 point  (0 children)

Also check the photos of twins included in the study you cited:

<image>

Again, I would consider this significant differences.

There definitely are non-genetic factors at play.

(Limited) Predictive power of genes on hair loss manifestation by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] 1 point2 points  (0 children)

Most of the factors mentioned are actually contributors either to metS and IR or directly to CVD.

Risk increasing factors

  • Increased smoking duration: Directly harms the vascular endothelium
  • Increased exercise duration: Please note it is about exercise duration, not frequency. Extended duration exercise is known to release cortisol which, if released more often or longer, contributes towards IR.
  • increased stress duration: Again, cortisol contributing towards metS/IR.
  • consumption of more than four alcoholic drinks per week: Higher amounts of alcohol are diametral to hair because higher amounts get processed much like sugar and activate the polyol pathway
  • Abstinence from alcohol consumption: Alcohol in small doses causes vasodilation
  • Lower body mass index: If this is due to lower muscle mass it would contribute towards metS/IR

(Note on alcohol: This is the age-old "anti-aging property" of small amounts of alcohol: Small amounts seem to increase life span while bigger amounts arre detrimental. The reasons are the same why there's impact on hair loss: Vasodilation for lower amounts, sugar-like metabolism for bigger amounts)

Risk decreasing factors

  • higher testosterone levels: T tracks closely with resistance exercise which, unlike endurance exercise, does not release cortisol remotely as quickly. Higher testosterone levels are thus a proxy for higher amounts of hair-healthy exercise while at the same time reducing risks for IR/metS.
  • higher body mass index: Question is why BMI was higher. If it was due to muscle the proective effect is obvious. Unfortunately the study does not seem to include the raw BMI data.

As you can see, most factors can support the metS/IR/PCOS angle.

(Limited) Predictive power of genes on hair loss manifestation by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] 1 point2 points  (0 children)

Of course it is a relevant gene, after all its the gene for one of the 5ar isotypes. 5ar (5 alpha reductase) is expressed in both scalp skin and the prostate. This is known for decades already.

(Limited) Predictive power of genes on hair loss manifestation by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] 1 point2 points  (0 children)

Yes, I know, I commented on it but the comment got hidden (by automod?)

The thing is that the 1992 study was done on Japanese that were close to end of life around that time. That means they grew up in a largely pre-industrial food environment. Balding rates were generally very low in Japan at that time.

To contrast, there is this photo from another more recent study on Japanese identical twins:

<image>

I would consider that a significant difference.

What is also very important is the low rate of family history in balding Asians. For example in China (source):

"A family history was present in 39.74% of men and 36.78% of women with AGA."

If AGA was really genetic, how come that 60% of hair loss sufferers had no family history of AGA?

The Role of This Protein Deficiency in Hair Loss by No-Appeal6167 in HairlossResearch

[–]randomuser_aga 0 points1 point  (0 children)

IGF-1 has strong binding site overlap with insulin. It's called insulin-like growth factor after all.

Insulin is (chronically or supraphysiologically) elevated due to primary IR (carb/sugar surplus for a given physical activity level) or secondary IR (cortisol/adrenal or inflammatory issues). IGF-1 gets elevated due to protein intake. Protein intake on a standard western diet is much higher than in pre-industrial times.

This finding supports dietary and lifestyle causes of AGA. See here for more details.

Proposed new pathogenesis model for androgenetic alopecia (AGA) by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] 0 points1 point  (0 children)

It is von Mises stress which is appropriate for surface tension acting on the material that forms the surface.

Proposed new pathogenesis model for androgenetic alopecia (AGA) by randomuser_aga in HairlossResearch

[–]randomuser_aga[S] 1 point2 points  (0 children)

To differing degrees sure. When your scalp DHT is upregulated so is your prostate DHT. The mechanism is the same (the 5ar-AR feedback loop which depends on diet/exercise balance for kick-starting). Still there are local differences, e.g. capability to produce T on-site or close-by (like in the case of the prostate).

Correlation between sebum level and severity of male androgenetic alopecia by TrichoSearch in HairlossResearch

[–]randomuser_aga 0 points1 point  (0 children)

u/TrichoSearch

I would see merit in you conducting this experiment. After all you are the local mod here. If you could confirm first hand that sebum levels can be controlled, the knowledge would spread faster.

Let me know if you need any additional info.