Checking NaN Values

NaN is a global property that represents an IEEE 754 “not a number”. (There is also a static NaN property of the built-in Number object, Number.NaN for pointless duplication (mdn)).

In older versions of ECMAScript NaN and other global properties like undefined were writable. You shouldn’t be doing that and Brendan, et al made it illegal; even throwin errors in strict mode..

The value type of NaN is “number”, as can be seen by the literal NaN property or by NaN values.

typeof NaN; // "number"
typeof (1 / "foo"); // "number"

Any value compared to NaN using the comparison operators == or === results false.

NaN == NaN; // false
undefined == NaN; // false

Method isNaN almost seems to work:—

isNaN(NaN); // true

— until it does type conversion, even attempting to run the algorithm when no argument is supplied.

isNaN(); // true
isNaN(undefined); // true
isNaN("-."); // true
isNaN(""); // false
isNaN("-2."); // false

The answer to that is to use Number.isNaN, which only returns true for actual NaN values and does not do type conversion.

Number.isNaN(); // false
Number.isNaN("1"); // false
Number.isNaN(""); // false
Number.isNaN("-."); // false
Number.isNaN("0xf"); // false
Number.isNaN("-2."); // false

Object.is can also reliably check NaN values:

 Object.is(NaN, NaN); // true
 Object.is(NaN, undefined); // false

Methods isFinite and the newer non-type-converting version Number.isFinite can work in certain situations:—

 Number.isFinite(NaN); // false

— but do not check exclusively for NaN, as they also return true for Infinity and -Infinity:—

 Number.isFinite(-Infinity); // false

But these methods are useful for numeric validation. Especially Number.isFinite, which, unlike global isFinite, does not do type conversion:

Number.isFinite("2"); // false
Number.isFinite(new Date); // false
isFinite("2"); // true
isFinite(new Date); // true

Teach Yourself to Speak

Have you considered learning English?

Your communication skills might not be as good as you think they are.

The greater burden of communication lies upon the one communicating the message. If you want to be understood, it is your duty to clearly and effectively communicate your intended meaning to your audience.

You don’t need school. All you need is your brain, a camera, and the will to speak well. Learn to speak by making videos of yourself speaking and watching them back.

LeetCode 54. Spiral Matrix in JavaScript

Problem

Given an m x n matrix, return all elements of the matrix in spiral order.

https://leetcode.com/problems/spiral-matrix/description/

Solution

https://leetcode.com/problems/spiral-matrix/solutions/2989475/four-pointer-javascript-video-demo/

Interactive Demo

https://mybanned.com//demo/spiral-matrix.html

Video

LeetCode 3. Longest Substring Without Repeating Characters — Interactive JavaScript

Problem

Given a string s, find the length of the longest substring without repeating characters.

https://leetcode.com/problems/longest-substring-without-repeating-characters/description/

Solution

Dynamic Programming Sliding Window with Set

Interactive Example using Promises

Explanation

Use a Sliding window. Go stepwise through characters of s to expand the longest unique string one character each step. Each time a new maximum size of characters in the Set is reached, it is stored in our variable, ans. The Set is used only to track the next possible longest unique set of characters.

If the next character in s is not in the Set, wordEnd is incremented, widening the window. Save ans = Max(new result, previous max).

If the next character is already in our Set, try a new window. We don’t know where in our word the next character exists, but we can try removing one char from the front of the set. This decreases the current running set of unique characters, but gives us a chance to possibly find a longer unique set.

MAX_LENGTH - wordStart > ans

If the length number of characters remaining are greater than our longest answer, continue the loop for a chance to get a longer answer.

Loop Terminal Condition

MAX_LENGTH - wordStart > ans
If the length number of characters remaining are greater than our longest answer, continue the loop (there is a chance to get a longer answer).

Time complexity

O(n)

Space complexity

O(2n)

JavaScript

function lengthOfLongestSubstring(s) {
    const MAX_LENGTH = s.length;
    const set = new Set();
    let ans = 0, wordStart = 0, wordEnd = 0;
    while (MAX_LENGTH - wordStart > ans) { // Loop terminal condition.
        if(!set.has(s[wordEnd])) {
            set.add(s[wordEnd++]);
            ans = Math.max(ans, wordEnd - wordStart);
        } else {
            set.delete(s[wordStart++]);
        }
    }
    return ans;
}

Changing while to do / while can improve performance. If the readability is good, why not use it?

Only one small tweak is needed to avoid an error. Can you spot the error?

function lengthOfLongestSubstring(s) {
    "use strict";
    const MAX_LENGTH = s.length;
    const testChars = new Set();

    let ans = 0, wordStart = 0, wordEnd = 0;
    if (MAX_LENGTH === 0) return 0;
    do { 
        if(!testChars.has(s[wordEnd])) {
            testChars.add(s[wordEnd++]);
            ans = Math.max(ans, wordEnd - wordStart);
        } else {
            testChars.delete(s[wordStart++]);
        }
    } while (ans < MAX_LENGTH - wordStart)
    return ans;
}

If s === "", its 0 property (wordEnd) is undefined.

We can avoid adding undefined to our map by doing a check for this special case before the loop.

if (MAX_LENGTH === 0) return 0;

Finally, adding "use strict" allows the script engine to make some of its own optimizations, more for sanity than performance. (This should mostly be done on the file level or by using modules or classes.) The result is readable and has phenomenal performance, beating 91.55 % of all javascript submissions.

Non-strict functions use a separate Environment Record for top-level lexical declarations. This is done so direct eval can determine whether any var-scoped declarations introduced by the eval code conflict with pre-existing top-level lexically scoped declarations. This is not needed for strict functions because strict direct eval places all declarations into a new Environment Record.

Performance: Beats 91.55%!

Criminal Artistworks, Lying Barry Shrum, OAG, Chinelo Bivens, Jennifer Urban, CCPA/CPRA 1798

In response to “offensive song lyrics”, Artistworks decided to remove me from their website.

In response, I requested my content back from them, including all videos and posts, per CA CC §1798.100.

Artistworks ignored all of my CCPA data portability requests to them.

I then filed a CCPA data portability request violation to the CA Office of the Attorney General (OAG) through the OAG’s website.

The OAG then reached out to Artistworks regarding the allegations I had made in my CCPA data portability request violation claim.

Artistworks responded to the OAG’s inquiry by deleting my data. Under legal representation by Barry Shrum, LLC, they then lied to the OAG, falsely stating that I had requested them to delete my data. I never requested this and it is not what I wanted.

Artistworks went on to further lie to the OAG, making libelous claims about me, a former student, in an attempt to justify their criminal actions.

Artistworks, of course, had no evidence to support their false claim that I had made the alleged request for them to delete my data. Their false claims simply didn’t happen. I had requested clearly, to Artisworks, in writing, they provide to me my data. Here is just one of the emails I sent to Artistworks. This email was addressed to Dawn Mendoza of Artistworks, clearly and lawfully requesting my data, per CCPA.

To: Dawn Mendoza <dawn@artistworks.com>,
Date: Jan 12, 2020.
Subject: CCPA Data Portability Request

Message:
YOU ARE HEREBY NOTIFIED OF LEGAL ACTION.

California Consumer Privacy Act (CCPA) Right of Access

You are to provide all of my data, including all media, posts, messages, and contacts in a human accessible and machine readable format, free of charge to me as specified by and provisioned for in CCPA SECTION 1. Section 1798.100 of the Civil Code. The data shall be in a readily-useable format that allows the me to transmit this information to another entity without hindrance.

In response, the OAG was supposed to fine them for their criminal activity, however, the OAG did nothing, accepting Artistworks’ defamatory comments as justification for their own inaction.





In follow-up with the OAG board, I asked the board “who holds the board accountable?” and “how does the board decide which cases to enforce and which to ignore?”. The board members, Jennifer Urban, et al, ignored that question.

In a follow-up to being ignored, I issues a FOIA request to the OAG for the video recording of that phone call. That FOIA request went ignored, as unfortunately happens with too many FOIA requests.

CCPA 1798.100.

OAG Public Inquiry Unit (916) 210-6276
Chinelo Bivens
PIU@doj.ca.gov

Jennifer Urban
jurban@berkeley.edu
Tel: 510-642-7338

Artistworks lawyer Barry Shrum, Esq (615) 338-5130

Pretextual Traffic Stops — Fourth Amendment Violation

The allowance for pretextual stops inevitably leads to fourth amendment violations.

Pretextual stops, or “looking for a reason” to initiate a traffic stop, by nature, form the basis for fourth amendment violations.

While it is possible that an officer could pull over an individual for a traffic infringement and happen to find suspicious criminal activity, that’s not usually how it goes down.

It’s important to differentiate happenstance observations during a traffic stop from pretextual stops, where the officer is actively looking for a reason to pull over a vehicle.

In Whren v. United States, 517 U.S. 806 (1996), the court determined that such stops were acceptable when it could be determined that “a reasonable officer would have stopped the car for the purpose of enforcing the traffic violation at issue”. This opened up barn-door wide leeway for officers who went above and beyond the court’s decision to profile, follow without cause, and use spurious reasons to pull over their target.

The latter form of stop, a pretextual stop, looking for a reason, provides officers with broad leeway to pull over drivers under the justification that the driver may have committed some infraction out of the almost uncountable number infractions on the books.

Such reasons can range from nitpicking license plate headlamp violations to reaching “dangerous lane change” and even speculative non-infractions such as “I couldn’t see if your seatbelt was on” stops.

Such pretextual stops can be identified when it is clear that the reason for the stop is poorly justified and the officer is looking for a reason to pull the driver over. They can be identified with the following characteristics:—

The officer either (a) did not clearly and immediately articulate the crime or infraction, (b) cited vague or spurious laws, (c) used reasons that occurred after initiating silent pursuit for the basis for the stop and did not articulate valid justification for pursuing the target, or (d) used insufficient evidence for the stop.

Such stops inevitably lead to fourth amendment violations and should therefore be ruled unconstitutional.

In the case of the video below, the officer began following his target before initiating a stop. The traffic stop had nothing to do with the officer’s unstated reason for following his target. The officer followed his target to “find a reason” to pull him over. Therefore, the constitutionality of the stop is questionable.

Any stop determined to be pretextual should be deemed invalid, thereby invalidating anything that came from the stop as “fruit of the poisonous tree”.

Optimize Mitochondrial Health for Overall Health

Overall health depends on mitochondrial health. Virtually all health conditions from physical and mental performance to cardiovascular health and aging are impacted by mitochondrial health. Optimizing it is therefore a powerful strategy to extend one’s healthspan, or longer quality of life.

Mitochondria are the powerhouse of the cell. They produce and release energy in the citric acid (krebs) cycle and the Electron Transport Chain (ETC).

Mitochondria are essential to cellular function. Cells cannot function without them. Mitochondrial dysfunction is implicated in diabetes, cardiovascular disease, stroke, concussion, and most neurodegenerative diseases. [Chistiakov][Jang]

Measuring Mitochondrial Health

As of 2021, health practitioners can’t test mitochondrial health, so they ignore it.

Commonly performed tests are inadequate. However, changes in overall health can be observed through better tests. Although these better tests don’t provide direct feedback on mitochondrial health, they do provide a more accurate representation of total health than the commonly prescribed, sometimes misleading tests.

Specifically requested performance tests can measure these values through indirect means. Tests such as blood glucose, kidney function, blood pressure, VO₂ max, and cardio IQ can give a rough indication of overall mitochondrial health.

Healthcare Diagnostic Failings

How Doctors Test Your Kidneys

Doctors assess kidney function by glomerular filtration rate (GFR), typically by an eGFR test. eGFR measures blood creatinine — that’s it — and uses fudge factor adjustments that include age, gender, race, and weight, as WebMD officiously explains. They use bodyweight to determine how much muscle you have (WRONG). The thinking behind this is that people have roughly the same ratio of lean body mass to adipose tissue (fat) (WRONG) and, since greater muscle mass leads to greater creatinine levels, heavier people must have more muscle (WRONG). Thus, heavier people with a higher GFR can be expected to be in good health (WRONG).

The eGFR test, which is practically useless for assessing kidney function, is a normal example of healthcare-industry turd-polishing. Be aware of this type of erroneous thinking, established into practice, look out for other such errors, and ask questions and seek answers.

Exercise increases creatinine, a metabolic waste product. And, since exercise increases liver enzymes, increased exercise might also indicate to your doctor that your kidneys and liver are in worse shape — more evidence to him that your new fad health regimen is just more quackery. And, if you’re also taking creatine monohydrate, that will also increase creatinine levels, leading to lower eGFR score, crudely indicating to your assumptive doctor that your kidneys and liver are in worse shape. Your doctor might even tell you to stop taking or doing whatever it is you are doing. Keep in mind, you own your health; your doctor is there to serve you. If you can’t get him to do that, find another doctor.

A better test of kidney function is a Creatinine Clearance test and an albumin/creatinine ratio test. These test circulating creatinine, urinary creatinine, and urinary albumin. Doctors don’t generally request these tests. If you want them, you’ll have to ask for them.

How Doctors Test Your Cardiovascular Health

Low Density Lipoprotein (LDL) particle number assessment is another widespread failing of modern health care. Calculating LDL-C is expensive for widespread screening so, as it is with kidney function, modern healthcare doesn’t test what they find to be “too expensive” and again performs a rough guesstimate.

The alternative to the widespread failure of lipid panel guesstimation is NMR spectronomy particle testing, such as Cardio IQ, which actually measures LDL levels, as well as their size and shape.

Heart disease is the #1 killer in the US, costing an estimated $363 billion dollars per year. That, however, has not stopped the healthcare industry from saving a few bucks by sticking to tradition and avoiding the slightly more expensive NMR tests which have been decreasing in cost over the past thirty years.

Although the best healthcare diagnostics are generally crude, improvements are being made. Get your doctor to work for you. DYOR, find the lab tests you want, communicate with your doctor, and listen to your body.

How Mitochondrial Health and Function can be Improved

On a cellular level, mitochondrial function can be improved in a few ways.

  • Mitochondrial biogenesis
  • Increased mitochondrial activity
  • Mitochondrial strength
  • Mitochondrial protection

There are several things you can do to affect those parameters. Understanding of their pathways is key to understanding what, why and how things work.

AMPK and PGC-1 alpha

The AMPK/PGC-1 alpha pathway leads to mitochondrial biogenesis and health.

PGC-1 alpha, the “master regulator” of mitochondrial biogenesis, regulates cellular energy metabolism and induces mitochondrial biogenesis. PGC-1a stands for PPAR Gamma Coactivator-1 alpha. PPAR’s regulate gene expression and PGC 1-a is a PPAR co-activator that regulates cellular energy metabolism. [Liang]

PGC-1 alpha can be activated by a number of things mentioned in this article. Anything that increases PGC-1a increases mitochondrial strength, number, and function.

Anything that increases AMPK increases PGC-1α. [Cantó], though AMPK does more than increase PGC 1-a.

AMPK or AMP-Activated Protein Kinase, is an enzyme that catalyzes the transfer of AMP to ADP to form ATP. ATP is a form of stored energy that is released in the citric acid cycle, forming ADP and AMP. When AMP/ATP or ADP/ATP ratios are too high, AMPK is increased. Increases in AMPK activation and PGC-1a lead to increases in mitochondrial DNA and mitochondrial strength and number.

Lance Hitchins does a deep dive into AMPK

NAD+ — Mitochondrial Fuel

Nicotinamide Adenine Dinucleotide (NAD+) is used in ATP production in the ETC. Think of NAD+ as fuel for mitochondria.

Synergy: Do Everything

Results come from consistent, total application. A halfway applied program leads to partial results. Most people will apply a small fraction of what little they understand and achieve a poor result. Although I explain what to do (exercise, supplements, peptides, etc), it’s up to you to do it consistently. And I’ve explained why and how, so that it can be understood, not followed on blind faith.

Exercise

Physical exercise is the best way to improve mitochondrial health and will have the greatest observable effects on overall health. Exercise should be at the core of any program. Exercise is the best way to increase AMPK.

Exercise increases PGC-1 alpha which stimulates mitochondrial biogenesis. Exercise also causes release of mitochondrial-derived peptides such as MOTS-c, a naturally-produced (more on MOTS-c below). Exercise strengthens mitochondria in all 3 muscle (skeletal, cardiac, and smooth) types, organs like the liver and kidney, and even nervous tissues of the brain. [Park][Steiner]

The most effective type of exercise for improving mitochondrial health is generally agreed to be high-intensity cardiovascular training at or above 75% maximal power (such as high intensity interval training (HIIT)). This is because PGC-1α expression at both the mRNA and protein level increases in an exercise intensity-dependent manner. Supplements, peptides, other approaches to improve performance can raise individual limits of beneficial HIIT. However, a conditioned response to HIIT decreases in benefit after more than 40 repeated bouts. [Bishop][Granata]

Intermittent Fasting

Intermittent Fasting (IF) is fasting between 12 to 24 hours. Several studies have reported significant reductions in body weight and fat mass with no significant changes in lean mass.

Fasting, like exercise, raises PGC-1 alpha. Intermittent fasting (IF) combined with high intensity interval training has synergistic effects suggesting increased mitochondrial mass. [Real-Hohn]

Cold Temperature

Cold exposure strongly induces a release of PGC-1 alpha and, as a result, induces mitochondrial biogenesis. [Chung]

Red Light Therapy, Photobiomodulation (PBM)

The wavelengths 660nm and 850nm increase ATP, increase mitochondrial membrane potential (for the ETC), and improve mitochondrial function in brain, muscle, eye, and organ tissues and, when used pre-workout, reduces post-workout creatine kinase levels. [Silveira][Eells][Keszler][Leal-Junior]

“[Photobiomodulation’s] principal player is the mitochondrion, whether its cytochromes are directly involved as a photoacceptor or indirectly through a vibrational and energetic variation of bound water: water as the photoacceptor.” [Ravera]

Whole body near-infrared (NIR) and IR before exercise increases mitochondrial membrane potential and ATP synthesis with a peak response at 3-6 hours. [Ferraresi]

Follow the instructions recommended by the device manufacturer, usually 20 minutes per day.

Fasted Training Strategy

Sleep early, rise early, do red light therapy for 15–20 minutes, train hard fasted, and then follow with cold or contrast hot/cold showers.

Mitochondrial Peptides Stack

Peptide Dose
5-Amino-1MQ 50mg daily for two months
Prevents breakdown of NAD+.
MOTS-c 5mg EOD for two to three weeks
Increases PGC-1α expression, attenuates insulin resistance, and enhances glucose metabolism via the AMPK signaling pathway. [Yang]
SS-31 0.5mg / kg bodyweight EOD for two to three weeks
Strengthens the cristae, the structures of the inner mitochondria where the ETC takes place. Reduces free radical production, improves exercise tolerance, and improves diseases stemming from mitochondrial dysfunction. [Campbell][Siegel]

Mitochondrial Supplement Stack

Substance Dose
NMN 500–1000mg daily
Increases NAD for energy in the electron transport chain (ETC).
PQQ 50–150mg daily
Stimulates mitochondrial biogenesis. Protects against exercise-induced fatigue and oxidative damage by improving mitochondrial function.
CoQ₁₀ Ubiquinol or Phytosome Q10 (Ubiqsome) 300-500mg daily
Generates ATP from metabolic products in the ETC. Protects mitochondria from oxidative damage and dysfunction.
r-ALA 100mg with larger meals
Reduces mitochondrial dysfunction and oxidative damage. Induces mitochondrial biogenesis. Complementarily promotes mitochondrial synthesis with ALCAR. Restores insulin sensitivity in muscle cells. [Shay]
ALCAR 500 – 1000mg pre workout or w/ carbs, 1-2x daily
Nutritively shuttles activated long chain fatty acids into the mitochondria (“carnitine shuttle”). Restores mitochondrial function and increases mtDNA.
Creatine 5-10g daily, w/ carbs
Increases ATP used in the krebs cycle. Prevents mitochondrial damage, increases mtDNA, and induces mitochondrial biogenesis.
Coleus Forskolin With large meals
Activates cAMP pathway for mitochondrial biogenesis, increased mtDNA, and mitochondrial activity.
Citicoline (CDP Choline) 1000mg prior to exercise
Strengthens mitochondrial membranes. [Rao]

Mitochondrial Peptides Detail

5-Amino-1MQ

5-Amino-1MQ inhibits nicotinamide N-methyltransferase (NNMT). NNMT is an enzyme that breaks down NAD+. Thus, inhibiting NNMT causes an increase in NAD+.

5-Amino-1MQ also activates senescent muscle stem cells, increases muscle recovery, and increase metabolism. [Neelakantan 1]

5-Amino-1MQ inhibits nicotinamide N-methyltransferase (NNMT). NNMT is an enzyme that breaks down NAD+. Thus, inhibiting NNMT causes an increase in NAD+.

5-Amino-1MQ has been shown to activate senescent muscle stem cells, and improve regenerative capacity of aged skeletal muscle, and increase metabolism. [Neelakantan 1][Neelakantan 2] [Neelakantan 1][Neelakantan 2]

MOTS-c

Mitochondrial Open reading frame (ORF) of the twelve S-c (MOTS-c) is a mitochondrially-derived peptide that responds to physical activity. MOTS-c regulates insulin sensitivity, physical capacity and performance.

MOTS-c is a peptide that improves physical function, insulin sensitivity, and metabolic disease states. MOTS-c is produced naturally in humans and is synthesized and sold as a peptide for research purposes.

Exogenous MOTS-c, combined with exercise, synergistically upregulates PGC-1α expression, attenuates insulin resistance, and enhances glucose metabolism via the AMPK signaling pathway. [Yang]

SS-31

SS-31 is a peptide found in the inner membrane of mitochondria, an area where free radicals are produced. SS-31 strengthens the cristae, the structures of the inner mitochondria where the ETC takes place.

Because SS-31 strengthens the inner mitochondria, it reduces free radical production, improves exercise tolerance, and improves diseases stemming from mitochondrial dysfunction. [Campbell][Siegel]

SS-31 restores healthy mitochondrial function, thus, it is primarily of benefit to aged individuals undergoing intense exercise training or those fighting T2D, Parkinson’s, or Alzheimer’s diseases. SS-31 has no effect on young, healthy mitochondria.

In 2021 study out of the University of Washington, researchers found NMN and SS-31 effective at restoring different aspects of mitochondrial and heart health, each through its own respective mechanisms. Combining the two resulted in a synergistic effect that rejuvenated old hearts to the young state. [Whitson]

SS-31 is also an orphaned drug, so, due to government control, it is not readily available for purchase.

These peptides can and should be synergistically complemented and potentiated with supplementation. Exercise is a prerequisite.

Mitochondrial Supplements Detail

Nicotinamide Mononucleotinde (NMN)

Niacin and its metabolite nicotinamide mononucleotinde (NMN) both increase NAD+ and mitochondrial NAD(P)H production under high workload. [Zhang][Whitson]

Niacin causes flushing (from prostaglandin activation) and blunts the release of free fatty acids (FFA). The flushing is uncomfortable but harmless, and reduced FFA release raises HDL. NMN does not have these effects. [Kamanna]

When niacin is metabolized, it uses a methyl group. This can be offset by supplementation of a methyl donor, such as 200–400mg Sam-e, B vitamins, trimethylglycine (betaine), or choline. All of these methyl donors have positive effects. Sam-e, in particular, restores intracellular GSH stores, especially in mitochondria. [Ming]

“Niacin, after undergoing biochemical reactions in the mitochondria with nicotinamide, and tryptophan forms nicotinamide adenine dinucleotide (NAD) and NAD phosphate (NADP). NAD and NADP are the active forms of niacin which, when reduced to NAD(H) and NADP(H) respectively, participates in catabolic redox reactions and are cofactors in anabolic redox reactions.” (sic) [Zhang][Whitson]

A 2019 study showed that supplemental NMN reduced levels of creatinine, a metabolic waste product. The mechanism of action is most likely improved kidney function as a direct action of NMN [Weiss]. Because overtraining and creatine supplementation can both raise creatinine levels, NMN is a perfect complement to creatine supplementation or any HIIT exercise regimen.

Pyrroloquinoline quinone (PQQ)

Pyrroloquinoline quinone (PQQ) is a naturally occurring coenzyme manufactured by bacteria, found in plants, and utilized by mammalian cells as an important nutritional growth factor. Because humans do not produce PQQ, this necessary nutrient must be ingested, either from scant amounts found in food, or via supplementation.

PQQ stimulates mitochondrial biogenesis through cAMP response element-binding protein (CREB) phosphorylation and increased PGC-1 alpha expression. [Chowanadisai]

PQQ also protects against exercise-induced fatigue and oxidative damage by improving mitochondrial function. [Liu]

In a 2020 study out of Texas, a small group of untrained men were split into groups. One group got 20mg PQQ per day, the other group got a placebo, and both groups trained on a stationary cycle.

The PQQ group showed greater weight loss and improved mitochondrial biogenesis by way of significant elevations in PGC-1a protein content. Although no advantageous improvement in aerobic exercise performance was found in the PQQ group, the authors attribute this lack of observed aerobic performance to the test itself; that fatigue kicked in before VO₂ max could be realized. Regardless, the weight loss demonstrated that PQQ, even when used alone, has observable effects. [Hwang]

In a 2016 study out of Japan, just 20 mg of BioPQQ™ per day improved cognitive function of elderly subjects. [Itoh]

PQQ was tested with no-observed-adverse-effect-level (NOAEL) at 100 mg/kg bw per day in a 90-day repeated dose oral toxicity study with BioPQQ™. (For a 50kg (110lbs) person, that comes to 5000mg PQQ).

Coenzyme Q10 (CoQ₁₀)

Coenzyme Q10 (CoQ₁₀) is used in the electron transport chain to generate energy in the form of ATP from metabolic products (sugars, fats, and proteins). CoQ₁₀ protects mitochondria from oxidative damage and dysfunction.

CoQ₁₀ administration increases brain mitochondrial concentrations and exerts neuroprotective effects. CoQ₁₀ and PQQ work synergistically with 5-Amino-1MQ to improve neurological function and increase energy turnover. [Matthews][Sarmiento]

Ubiquinol, the reduced form of CoQ₁₀, has shown superior uptake to ubiquinone. Because ubiquinol is fat soluble, it should be taken with fat. [Zhang, Ying]

Phytosome Q10, a lipid-soluble form of CoQ₁₀, has demonstrated higher bioavailability and increased mitochondrial functionality in cultured cells. [Rizzardi

Creatine Monohydrate

Creatine increases power output by increasing ATP. ATP is used a few ways in energy production, including the citric acid cycle and the electron transport chain, both of which occur inside the mitochondria. [Cooper] (See also: How the mitochondria produces ATP in steps.)

Creatine protects mitochondria from damage, increases mitochondrial DNA (mtDNA), and induces mitochondrial biogenesis. This explains why creatine has been evidenced to fight the effects of aging. [Gowayed][Barbieri][Candow]

Coleus Forskolin

Coleus Forskolin activates the cAMP pathway inducing mitochondrial biogenesis, and increasing mtDNA and activity. [Bogacka]

Racemic Alpha-Lipoic Acid (r-ALA)

Alpha-Lipoic Acid (ALA) reduces mitochondrial dysfunction and oxidative damage. ALA protects cells, including neurons, from damage, and induces mitochondrial biogenesis. [Shen][Nutritionreview.org][Fernández-Galilea][Shay]

Sodium r-Lipoate (Na-r-ALA), the Best Form of ALA

Racemic ALA, or r-ALA, is the reduced form of ALA. r-ALA has shown significantly higher absorption than the synthetic S- form (s-ALA). Most commercial formulations use a combination of s- and r- enantiometers because it is cheaper to do so, but do not specify this. [Streeper]

Sodium r-Lipoate (Na-r-ALA) is less prone to polymerization (“gunking up”), is completely soluble in water, and displays much better absorption. [Carlson] Always use Na-r-ALA.

Acetyl L-Carnitine (ALCAR)

Carnitine directly affects mitochondrial respiration. It transfers activated long chain fatty acids into the mitochondria in a series of reactions called the “carnitine shuttle”. [Ferreira]

Carnitine spares glycogen and burns fat during exercise. The form Acetyl L-Carnitine (ALCAR) has the advantage of crossing the blood-brain barrier to reach the brain and improve neurological health and function. [Wall]

References

});

window.addEventListener(“hashchange”, (ev) => {
const el = location.hash && document.querySelector(location.hash);
setTimeout(()=> el?.scrollIntoView({behavior: “smooth”, block:”center”}), 100);
});

YouTube Censors The NIH in Comments

YouTube Censors any links to the NIH website, including NCBI, PubMed, and all others. Any links to the NIH are censored from youtube comments.

To test this feature:

  1. Visit https://youtu.be/b04ty1cWj-E
  2. Add a comment linking to the following article:—
    https://www.nih.gov/news-events/nih-research-matters/lasting-immunity-found-after-recovery-covid-19
  3. Wait for a minute, then refresh the page

If your comment disappears, then you’ve been effectively prevented from sharing dangerous science.

Emerging Adults

The duration of human maturation now includes an additional 4–6-year pre-adult period. “Emerging adulthood” is used to explain problems of delays in learning about intimacy and mutual support, socialization, and the attainment of social skills needed for mating and reproduction.

Social scientists contend that the period of emerging adulthood has an “evolutionary context” and cite developmental markers as evidence to support the rapidly growing consensus of the hypothesis that post-adolescents require protection as they are still learning and maturing.

Society, with poor understanding of personal development, influenced by dogmatism and false beliefs, is producing children in a way that is not well optimized. It doesn’t seem to be getting better, either. Rather, it seems to be going in the opposite direction, towards inhibition of maturation.

Modern psychology’s new developmental phase, “emerging adulthood”, describes individuals who did not not socially mature but have reached biological maturation. It is a way of further categorizing people into age groups to explain the effects of predefined stations in life.

Looking for something to attribute this phenomenon, social scientists point to the further development of the prefrontal cortex that continues to develop into the early twenties. This single-factor hypothesis has scientific consensus.

But how can they be so sure that they’re correct? How did they rule out developmental socialization as a factor?

During early college years, emerging adults exercise freedom they have never experienced. Many find themselves in out of control situations, drunk, hurting themselves and others, exhibiting behavior that does not quite fit the definition of informed consensual sex.

Is this harmful behavior explained solely by underdevelopment of the prefrontal cortex, as the social scientists claim, or could the social skills be addressed by better socialization and enculturation?

Early college students also show increased demand for psychological services. Are they inadequately adjusted? And if so, can that be helped by better socialization?

Social conditions in adolescence, compared with other stages of life, have unique effects on brain and behavior that can last a lifetime. During adolescence, the brain can be developed to acquire tasks more suited towards that phase of brain development. The parts of the brain that undergo most change during adolescence govern internal control, multi-tasking and planning, self-awareness and social cognitive skills, and the understanding of others.

Traditional model of schooling and obedience prevent such skill development. This system is also not suitable for disagreeable persons, which is why it favors girls who are more agreeable than boys.

The same social scientists that point to the prefrontal cortex as a single factor cause of their newly-coined phase “emerging adulthood’ also either don’t acknowledge the fact that physiological maturation starts earlier than it did in the mid-1800’s or they do acknowledge that and claim that it’s a bad thing, warning of the dangers of “early puberty” or the more pathological-sounding “precocious puberty”, natural phenomena which they blame on obesity or hypothetical overexposure to harmful EDC’s.

Archaeological evidence shows that in modern humans, from 10,000 years BCE to the mid-1800’s, the age of onset of menses rose by roughly 6 years fro age 10 to over age 16, and has since returned closer to where it should be naturally, with good sleep and nutrition.

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Menarche age over the last 12,000 years. The age of menarche gradually increased until the recent secular trend’s decline, as shown in Figure 3. Evolution, development and timing of puberty – PubMed

Menses comes with hormonal maturation and is accompanied by development of neural networks in the brain.

The physical maturation of the brain is beginning closer to where it should be, at earlier ages, closer to where it was in the Paleolithic man. Brain maturation now begins in earlier life years, closer to where it was 10,000 years BCE. This can be attributed to better health and nutrition.

Researchers have observed that maturation extends later into life, into the mid 20’s, a period of continued maturation, not a loss of ability.

Over the past 10,000 years, human brain size also decreased, another phenomena that can be explained by diet.

Yet as brain maturation begins earlier, requisite social skills are not being concordantly exercised and developed. Children are being overprotected and prevented from developing, capturing helplessness and sealing it into the physiological development of the brain.

As physiological onset maturation improved, social and mental development worsened with neglect. Yet this phenomenon of delayed maturation is being attributed to and explained by the hypothesis related to new discoveries of neurological development.

What is the error correction mechanism? Who will be the changers? Overprotected and controlled children? Emerging adults? Where does the overprotection from “harmful ideas” end?

In the last decade, from 2011 to 2021, we have seen a drastic increase in censorship and a loss of privacy. There is an increase in the social need for psychological safety shown on platforms like facebook that protect against speech deemed “offensive”. Rather than moving in the direction of mental toughness, we are overprotecting to create fragility.

Keeping kids in protective bubbles while their brains develop physically does not give them the skills needed for mating and reproduction. Rather, protecting kids from interpersonal activities prevents them from developing the skills needed to thrive as humans — skills they desire to exercise — often against their consent.

A good parent is a good mentor. They observe the strengths, inclinations, aptitudes, interests, and weaknesses of their children to help them develop, apply themselves, and find teachers.