Metabolic Thresholds – The Importance of Dose & Schedule

Warfarin_ball-and-stick_model

Rat poison is Warfarin, so what benefit could it be to humans? At the correct dose and schedule it can treat blood clots and acts as a blood thinner beneficially.

From Wikipedia:

Warfarin, sold under the brand name Coumadin among others,[1] is a medication that is used as an anticoagulant (blood thinner).[4] It is commonly used to treat blood clots such as deep vein thrombosis and pulmonary embolism and to prevent stroke in people who have atrial fibrillationvalvular heart disease or artificial heart valves.[4]

What is of more relevance is that almost all substances with an active ingredient have the same properties to a varying degree. In the same way if you were to drink half a glass of wine daily it would probably be advantageous to your health as the body can metabolise alcohol at a low dose, but take too much quickly and it acts as a toxin. Staying below the metabolic rate can turn vice into virtue in terms of it’s effect on the body.

Before 1914 in America all drugs were allowed and when current drug policies were recommended the medical establishment responded by explaining that this was an attack on generic [ patent expired ] medicine. It was already established that cocaine-hydro-chloride was the most effective treatment against melancholia (now known as depression).

If you’re wondering why the “sky did not fall” when these drugs were legal, it’s because when something is legal it’s issuer is liable and this helps to ensures that providers only sell drugs within their metabolic threshold and that accurate information is provided (if the correct framework is in place).

Additionally at the correct dose and schedule receptor loss was not experienced which is what creates the debilitating side-effects if taken at a higher, toxic dose. Metabolic rates were issued in accordance with BMI [ Body Mass Index ] and metabolic threshold was determined by multi-regression, measuring long-term receptor loss. What this plot and line of best fit established is that receptors only denature when a toxic dose is reached.

Other medications that were used before prohibition of drugs also reveal:

1280px-LSD-2D-skeletal-formula-and-3D-models

  • LSD (Lysergic Acid Diethylamide) at low dose increases neuro-plasticity (the brains ability to learn new information) and is only a hallucinogen at a dose orders of magnitude higher than what is needed to improve memory

Cocaine-from-xtal-1983-3D-balls

  • Cocaine-Hydrochloride at a low dose (that takes about a month to accumulate in the human body) is an effective antidepressant,  performance enhancer (increases memory, focus, drive, and hand-eye coordination and performance in sports) and was included at a dose of 9mg / bottle in Coca-Cola for nearly a century.

Heroin-from-xtal-horizontal-3D-balls

  • A low but regularly administered dose of Heroin (Diamorphine) helped patients recover faster from emotional pain, whereas morphine was found to be more effective for physical pain. It was widely used for patients who were experiencing bereavement before prohibition. The metric used to determine its proficiency was days absence from work after bereavement of spouse or child. I think that’s about as objective a metric as can be used.
    800px-methamphetamine2
  • Methamphetamine  [ sold as brand name NoBull™ and was available in any quantity before prohibition; Cattle Tranquilliser added to water ] is a chemical compound that binds to and activates both sigma receptor subtypes, σ1 and σ2, in the brain and like it’s chemical cousin Methylphenidate (Ritalin) blocks the dopamine transporter resulting in accumulation of FOSB if taken above the metabolic rate which determines its toxicity. Adjusted to the correct potency it also treats ADD and was used for the same purpose before it’s more newly patented alternative Methylphenidate (Ritalin) became the approved treatment (formerly Methamphetamine was used because it was more effective and had less side effects adjusted for efficacy but its also true that it was used far less and was not as heavily marketed). Dose and schedule for both Meth’s determine toxicity and both can be taken without major long term side effects if taken below the metabolic rate and act as a stimulant increasing concentration. It appears that the one with an active patent received more political support and the generic got outlawed. Can you guess why?

Current policy is possessed by a black and white thinking fallacy that drugs are either good or bad rather than determining at what dose and for what condition to determine what is advisable. It’s kind of like asking whether shiny metal objects are good or evil – more needs to be known before we can establish what would constitute sound discernment.

How did we get into this mess? There is a clinically bad interaction between money and medicine in the current system.

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I did my research and came to a similar conclusion several years ago. It’s amazing to see such videos come into being and gives me hope that this planet is still capable of being objective in some amount.

– George

George Molson
Founder of ANTEKK

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1974 Medical Study – Cannabis Cures Cancer

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Cannabis in scanning electron microscope

Injecting mice with lung cancer with cannabinoids retarded tumor growth. The effect was dose dependent.

marijuana
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The National Cancer Institute did a follow up study in 1975:

 1975 Sep;55(3):597-602.

Antineoplastic activity of cannabinoids.

Abstract

Lewis lung adenocarcinoma growth was retarded by the oral administration of delta9-tetrahydrocannabinol (delta9-THC), delta8-tetrahydrocannabinol (delta8-THC), and cannabinol (CBN), but not cannabidiol (CBD). Animals treated for 10 consecutive days with delta9-THC, beginning the day after tumor implantation, demonstrated a dose-dependent action of retarded tumor growth. Mice treated for 20 consecutive days with delta8-THC and CBN had reduced primary tumor size. CBD showed no inhibitory effect on tumor growth at 14, 21, or 28 days. Delta9-THC, delta8-THC, and CBN increased the mean survival time (36% at 100 mg/kg, 25% at 200 mg/kg, and 27% at 50 mg/kg, respectively), whereas CBD did not. Delta9-THC administered orally daily until death in doses of 50, 100, or 200 mg/kg did not increase the life-spans of (C57BL/6 times DBA/2)F1 (BDF1) mice hosting the L1210 murine leukemia. However, delta9-THC administered daily for 10 days significantly inhibited Friend leukemia virus-induced splenomegaly by 71% at 200 mg/kg as compared to 90.2% for actinomycin D. Experiments with bone marrow and isolated Lewis lung cells incubated in vitro with delta9-THC and delta8-THC showed a dose-dependent (10(-4)-10(-7)) inhibition (80-20%, respectively) of tritiated thymidine and 14C-uridine uptake into these cells. CBD was active only in high concentrations (10(-4)).

PMID:
1159836

Some people have trouble reading medical literature. Here’s what they are saying:

Lung cancer growth decreased when mice were fed: delta9-tetrahydrocannabinol (delta9-THC), delta8-tetrahydrocannabinol (delta8-THC), and cannabinol (CBN), but not cannabidiol (CBD)

After 10 days the tumors growth slowed down depending on dose given. After 20 days primary tumor size decreased.

Cannibinoids were effective in treating one type of leukemia (friend) but not another (murine leukemia)

Verify that what I am saying is true:

https://www.ncbi.nlm.nih.gov/pubmed/1159836

See Also:

Emerging Clinical Applications for Cannabis and Cannabinoids: A Review of the Scientific Literature.