Tag Archive for: Medication

Resistance vs Tolerance in Neurodivergence

Pharmaceuticals’ info on Medication is always generic.

Pharmaceuticals will never disclose specific details to consumers and doctors for marketing purposes, most notably Meds-lifespan.
Patients are the first to acknowledge, after few weeks, what professionals don’t say, to their dismay.

There’s no such general consensus on the duration of medications.
Doctors know it.

The lifespan of meds as indicated by manufacturers, is calculated  ‘on body at rest’ and always averaged.
It is mostly unlikely that someone will take a medication in a state of wellbeing.

The current trend in psychopharmacology is XR, as in Extended Release.
XR is calculated in 12 hours, though in real life, the compound is often metabolized within 10 to 6 hours.
This is what defines  “Resistance”, a synonym of Metabolism.

There are hundreds factors affecting Metabolism however, let’s not overlap reactions.
Metabolism is the body Absorbing process of food, vitamins, minerals, medications… its timing varies in each individual.

Stress speeds up metabolism dramatically, the body desperate reaching-out for energy in all directions, last but not least, medication.

I see Tolerance as a bypass of Resistance, not Addiction.
When we get the full benefits of a substance, we don’t develop Tolerance.

I hear all the time from patients: “My medication stopped working”, in contrast to “I’ve been on the same med for 20 years and it works like the first day”.
Since we’re focusing on Mental Health, I ll describe the latter comment as in Mood-Stabilization, hardly achievable for working people in our constant challenging society, though not impossible.
Stable Mood is the criteria used by pharmaceuticals in order to set a med’s active status.
This is very misleading to individuals in leadership positions or students facing challenges on a regular basis. There are ordinary days when meds last longer, or hectic times when they don’t work at all. 
Cortisol and Adrenaline are the main culprits for pushing Metabolism into overdrive.

With that said, what’s the remedy?

Antipsychotics are the only compounds known to slow down Metabolism with side-effects like Weight-gain and Sedation.

More research is needed.

My takeaway is adjusting dosage according to situations.

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Fatigue in ASD/ADHD

Medical science cites 6 hours as the least amount of sleep in a 24 hours period. Autistics may well need 8/9 hours. Sleep affects medication and performance.

It is proven that autistics get more tired than the average person.
This is easily understandable since every task requires extra planning and decision making.
I need at least 8 hours of sleep to function, while 4-5 hours is the norm these hectic days.
People pretend to get used to it, despite evidence having long shown how lack of sleep weakens the Immune System and shortens life-expectancy, yet I often feel ‘lazy’ even if I put up long hours at work.

Fatigue is not laziness.
My cause of Fatigue is Anxiety, which in turn triggers Insomnia.
Insomnia is debilitating to me.
That leaves me with two options: double up my meds or call in sick. 
The former is the most likely, though not without consequences the likes of hypertension, encephalitis.
Thus far for ADHD meds.

Avoiding triggers and proper rest is paramount for all.
Regular sleep is crucial in Mood-stability.

Stimulants are the meds of choice for ADHD through enhancing dopamine, the main neurotransmitter involved in reward and motivation.
Reward and motivation have an antidepressant component.
People with ADHD must take them anyhow for studying or working.

Mood-stabilization is the ultimate goal.
We’re still far from it: antipsychotics remain the only option to date.

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Self-identification vs Empathy and anticholinergic therapy in autism

Medications reach maximal adherence in synergy.

These two emotional states may look equal despite the mechanism of action being of different contexts.
Self-identifying is of hormonal origin, mainly adrenergic.
Empathy is of brain-circuitry origin, a kind of personality.

Autistics score high on self-identifying.

Endorphins overdrive is the most common reaction normally leading to meltdown in distressing situations.
It is established that adrenaline’s release through endorphins is contagious and autists have highlighted senses causing them to absorb it all.
Hormones play a pivotal role.

As for reward, we all crave for it: reward enhances dopamine and serotonin, the ‘feel good’ neurotransmitters.
These chemicals are often dysfunctional in autism.
Hormones affect neurotransmission to a varying degree.
In my experience, I don’t feel rewarded most of the time.

Off-label treatment is showing promising results, although the placebo effect cannot be ruled out.

Acetylcholine is the main neurotransmitter present at all body s nerve endings.
It plays a key-role in memory, motility, metabolism.
All neurotransmitters are somehow dependent to acetylcholine.

Anticholinergic therapy mimics the model of action of antidepressants by blocking neurotransmission at pre-synaptic level.

Latest research shows anticholinergic optimal response in combination with antihistamines and benzodiazepines.

In hot-humid climates, anticholinergics are widely employed in Motion-sickness by targeting Neuronal-displacement, coincidentally responsible for autistic meltdown.
In my experience, they have calming and non-sedating properties.
Specific categories of drugs peak efficacy in synergy. 

Meds’ info generally highlights Warnings of “potential interactions” or “no interactions reported”, thus far creating further apprehension among users. 

It is important to understand what the targets of drugs are.

  • Anticholinergics: acetylcholine 
  • Antidepressants: serotonin, dopamine, noradrenaline 
  • Benzodiazepines: G.A.B.A.
  • Antihistamines: mast cells’ histamine released in response to allergic reactions 

These compounds interact safely.

We know that most current medication cures symptoms, not the original disease.
We must identify where the symptoms originate in order to understand interactions, what meds-info will never tell you.
The Internet is all the more misleading and partial with countless medical ads.
Medical textbooks are mostly reliable.

Let’s start with Acetylcholine:
Acetylcholine is the final product of the Parasympathetic Nervous System.
That would explain the anticholinergics’ enhancement of anti-allergens like antihistamines.
For this reason, Acetylcholine is also referred to as neuromodulator.
Needless to say, the parasympathetic nervous system reverts allergic reactions triggered by the sympathetic nervous system.

Humoral neurotransmitters:
Serotonin, Dopamine and Noradrenaline are released by brain synapses following an electric impulse through neurons. 
Cerebral electric-activity determines functional neurotransmission and mood.
Antidepressants increase humoral neurotransmitters activity.

G.A.B.A.
Benzodiazepines enhance Antidepressants targeting the calming neurotransmitter GABA.
GABA in turn, is highly involved in the regulation of electrical nerve impulses.
See the interaction of benzodiazepines with electric-activity and anticonvulsants in the cure of epilepsy, an electric signals dysfunction.
Benzodiazepines increase GABA activity.

Histamine:
Histamine is released by mast cells present throughout the body.
Their function is to fight inflammation.
Inflammation is the response to allergens affecting mainly skin, airways and gastrointestinal tract.
The controversy of histamine is that it exacerbates inflammation.
Antihistamines block histamine release.
Their mechanism of action is not fully understood: they are potentially drowsy, sedating, enhancing all aforementioned compounds.
For this reason they are often used off-label in mental health.

Speculation that mental illness may be an allergic reaction is taken into consideration.


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