Friday, May 8, 2015

Orexin , Interleukin , Inflammation, Laser Led

depression can  be caused by IL-1 (R, R2), and it may be the cause of your shitty moods. 

IL-1 also causes fatigue by suppressing orexin

IL-1beta is increased by Sleep deprivation (R), Smoking(R), Excessive glucose/sugar (R) and Alcohol


Top Choices To Decrease IL-1beta

Top Functional Foods/Condiments

Top Devices and Lifestyle


  • LLLT  (R)
  • Fasting (R) (Increases IL-1Ra)

Top Supplements

Foods To Decrease IL-1beta

In general, vegetables and fruit should help decrease IL-1b.
  • Cyanidin-3-O-β-glucoside (C3G) – typical anthocyanin (R) – found in many fruits
  • Ginger (R) – has lectins, but was one of the most potent out of 20 medicinal plants (R)
  • Sulforaphane/Broccoli sprouts/Cruciferous Vegetables (R),
  • Anthocyanins (from red raspberries) (R)
  • Oat polyphenols (R),
  • Astaxanthin in fish (R),
  • Betalain/Beets (R),

Other IL-1beta Decreasers



In rats, exposure to 4 degrees C or 39 degrees F  increased TRH release by 2 fold in the first 15 min.
Therefore you want to expose yourself to cold by going outside in the winter or taking cold showers.  This means to completely turn off hot water.  I can only do this one minute or else it’s too annoying.
You can additionally take Hypothalamus glandular, which probably contains some minute concentrations of TRH.  Take 1500mg per a time.

19) Molecular Hydrogen/Ghrelin

Consuming hydrogen-rich water is a potent antioxidant and, like LLLT, seems like a panacea (R).    I use a machine to produce hydrogen rich water, but you can also do it with hydrogen sticks(haven’t experimented with the sticks).
Hydrogen rich water likely increases orexin, since it has been found to increase ghrelin (R).   Ghrelin increases orexin (R).

20) Acetylcholine

Acetylcholine MOSTLY  increases orexin (R).  It can inhibit it simultaneously through a different mechanism, but it mostly increases it. (R)   I recommend Alpha GPC.

21) ATP

Increasing ATP levels can increase orexin. (R)
The following increase ATP: Lactate, LLLT, Methylene Blue, mTOR activation, Oxygen, Acetylcholine (R), CES, CoQ10, Lipoic acid, Ribose, Glucose, Pyruvate, Carnitine, Uridine, Bicarbonate, Malate, Creatine

22) Hypothalamus Glandular

Neurotensin is a hormone found mostly in the hypothalamus and regulates luteinizing hormone and dopamine pathways. (R)
It also decreases our body temperature and pain levels and increases our energy (‘locomotor activity).  It also has important gut functions. (R)
I would put Hypothalamus glandular under my tongue.  I have done this and it seems to have an effect.

23) Caffeine

Caffeine was found to activate orexin, which isn’t surprising. (R)
I recommend getting your caffeine from Jasmine Tea.

24) Pregnenolone and Other GABA Antagonists

GABA antagonists or ‘negative modulators’ block the effects of GABA.
GABA suppresses orexin, so blocking GABA will help activate it.  My subjective experience validates this.
The most powerful substances here is pregnenolone.  I’ve gotten decent wakeful promoting effects from Zinc, Chocamine, Ginkgo, Muira and Wormwood (be careful).
  • Pregnenolone (R, R2). ‘Potent’.  I use 25mg, but you can start with a lower dosage. I and all of my clients find this helpful in promoting wakefulness. (gamma2-subunit independent)
  • Progesterone (R) – Pregnenolone converts to this, so I just recommend pregnenolone.
  • DHEA (R) +DHEA-S (R) – Pregnenolone converts to this, so I just recommend pregnenolone.
  • Ginkgo/Bilobalide and Ginkolide (R, R2).  This extract should contain about 2% bilobalide.
  • Zinc (R) (different mechanism than pregnenolone -gamma2-subunit)
  • Wormwood/Thujone (R)…Thujone is also found in sage.
  • Muira Puama (R)  – I needed to take 4 pills to significantly feel the wakefulness.
  • Chocamine/Theobromine and Tea /Theophylline (R)
  • Naltrexone – low dose won’t likely have a significant effect.
LASER LIGHT LED 

Where To Use It On The Head

  • Front of the head for Increased focus and increased analytic ability
  • Upper and side portions of the head for creativity
  • Limit usage in the back of the head where the occipital cortex is.  Maybe do a third of what you do in the front of your head.  If you have CFS then do it in the back, as there’s evidence that CFS is as a result of brain stem inflammation.

Other Places I Use it

I mainly use it on my brain, but sometimes other locations.
  • Sports injuries/other injuries.  I’ve had one on my finger, my shoulder, etc.. (Effective)
  • I use it rarely on my thymus to increase my immune system and immune tolerance (used it maybe 20 times in total) (Effective)
  • I use it rarely on my thyroid to increase thyroid hormones (used it maybe 20 times in total) (Effective)
  • I use it rarely on my liver to increase liver regeneration (maybe 15 times total) (Effective)
  • I use it rarely on my stomach to increase stomach acidity, GI repair (maybe 10 times).  (Effective)
  • I use it in my teeth to increase dentin.  One tooth has some dentin that’s been worn away.  (Effective)
  • I’ve used it once on my testes to increase testosterone.  I’ve only used it once there because I’m a bit scared to use it there as I don’t understand its interaction with sperm enough. (Unable to determine effectiveness.)
  • I use it sometimes on the side of my face to heal nerve damage as a result of bells palsy as a kid. (Effective)
  • Massive sting.  I was recently attacked by a flying creature that was massive – bigger than a queen bee.  It attacked a spot in my foot and injected a poison that caused a large portion of my foot to swell.   I put LLLT on it and it practically disappeared in like 2 days.
  • Although I don’t use it for my skin, it can very well be used for it (R)
  • I have not used it for this, but if you get hemorrhoids you can place this laser pointer up your rectum.

How To Use It

I recommend using this before bed, as it causes fatigue in many.  I believe the mechanism is by increasing TNF-alpha acutely (R).  While it may acutely increase TNF-alpha, it down-regulates the production chronically (R).  Read my posts about how inflammation and TNF-alpha is related to fatigue.
First use: Place on each spot on the head for 10 seconds and switch to a different spot.  Cover the whole head, except the back.  Total time should be 2 min.
Second use: If you felt tired after the first usage then continue at that dosage for a week.  If not increase by 10 seconds to a total of 20 seconds per a spot and 4 minutes in total.
If you feel tired and groggy the next day, you had too much.  If not, keep on increasing the dosage by 10 seconds until you hit 2 minutes per a spot and a total of 15 minutes.
If you feel groggy the next day and only took 30 seconds per a spot (less than 6 minutes in total) then it means you have an inflammatory and/or mitochondrial issue.  LLLT will help with it.
If you feel tired after 2 minutes of putting it on your head this also means you likely have an inflammatory and mitochondrial issue.  Again, LLLT will help with it.
Use every other day.  I recommend every third day if you’re generally functioning pretty well.  If you’re taking  a lot of other supplements then use once a week perhaps.  That’s what I do.  The benefits are abolished if used daily for a few weeks.
An alternative way of using it is to put it on your head in the day time for two minutes in total.   This isn’t enough to make most people tired, but it still stimulates Cytochrome C Oxidase.  I would definitely recommend using it this way if your sleep is disturbed by LLLT.
Last, don’t worry about the detailed instructions or screwing up.  This is very safe if you use it even somewhat right.  The reason I give these instructions is so that people with underlying inflammatory issues aren’t scared off if they see some negative effects.

When Will You See Results?

LLLT is like exercise  – benefits are accrued and realized after the healing stage, but there’s usually a noticeable effect the next day.
If you don’t notice anything from laser therapy then congratulations – you likely have healthy mitochondria and low levels of inflammation

LLT LASER LED RED/BLUE Effects Experience

  • Increases higher order cognitive function
  • Improves memory via growth factors and brain metabolism (R,R2)
  • Improves attention (R)
  • Improves working memory (R)
  • Improves mood (R)
  • Improves motivation
  • Increases wakefulness
  • Increases sports performance (via sensory and motor improvements) (R)
  • Decreases need for sleep

LLLT:
  • Suppresses inflammation: PGE(2), Cox 2, IL-1b, TNF, IL-8, IL-6, neutrophil cell influx, etc.. (R, R2, R3)
  • Increases internal antioxidants (SOD) (R)
  • Decreases free radicals and oxidatively stressed neurons (R)
  • Increases brain Hypoxia-inducible factors (HIF-1α) and vascular endothelial growth factor  (VEGF) (R).   HIFs are normally increased under low oxygen conditions.  This is the body’s stress response.  HIF-1 increases several genes to promote survival in low-oxygen conditions. These include enzymes that allow ATP (cellular energy currency) synthesis in an oxygen-independent manner, and VEGF, which promotes the formation of new blood vessels (angiogenesis) in the brain.    This makes sense because when the brain is starved for energy it will try to make up for it.
  • Increases stem cells (R, R2, R3)
  • Increases Nerve growth factor (NGF) (R)
  • Increases Brain-derived neurotrophic factor (BDNF) (R)
  • Increases Neurotrophin-3-contradictory (NT-3) (R)
  • Increases IGF-1, TGF-b (R, R2), PDGF, FGF2 (R)
  • Increases ATP production (R)
  • Increases the number of mitochondria (R) i.e mitochondrial biogenesis
  • Promotes the synthesis of DNA and RNA (R)
  • Increases neuronal mitochondrial metabolism byphotostimulation (stimulation by light) of an enzyme (cytochrome oxidase) involved in increasing mitochondrial oxygen usage (R) and increases mitochondrial membrane potential (R)
  • Increases blood flow and circulation (R)
  • Decreases amyloid-β aggregates in human brain cells (in-vitro) (R), the protein responsible for Alzheimer’s.
  • Activates PKC (R)
  • Upregulates heat shock proteins (R)
  • Stimulates mast cell degranulation (R)
  • Modifies extracellular matrix components (R)
  • Prevents neuronal death by greater membrane stability and resistance to depolarization, which has been shown to transiently reduce neuronal excitability (R)
  • Prevents cell death, improves cell proliferation, migration and adhesion (R)
  • Increases the expression of genes in the brain by increasing the transcription factors Nf-kb (R), AP-1 and CREB (R). Transcription factors are proteins that bind to DNA and supports growth and repair.  See this video animation on how these proteins bind to DNA.
  • Increases our body’s natural opioids (R).
Interestingly, in normal neurons LLLT  increased oxidative stress/ROS. In oxidatively-stressed cells LLLT reduced high ROS levels and protected cultured cortical neurons from death (R)
Some of the mechanisms are similar to methylene blue.  

LLLT Goes Well With

http://www.foodservicedirect.com/product.cfm/p/209683/Berlin-Natural-Bakery-Sourdough-Spelt-Bread.htm?gclid=CjwKEAiAnqWkBRCGm5uyu5r13jsSJACBZ4Wy8_Sn9AqEPoycJK_x-YJ5OM1IdJkkIXqjz1KN0XAgjhoCmUzw_wcB

26) Forskolin

Forskolin is a well known wakeful promoter and it certainly produces a noticeable effect with me.
Forskolin increases cyclic AMP in the whole body, including in the area where orexin neurons are.   This causes these neurons to activate (long term potentiation) and the result is we’re more wakeful. (R)

I am convinced GHRP 2 , MOD 1-29 and CJC-1295 will help and reverse age related decline in cognition, promote delta wave sleep and increase muscle mass verse fat

GHRH last for 30 minutes or more. This is a fine peptide to contribute to a GH pulse. This I call modified GRF(1-29)

Somatostatin is stopped by GHRPs     very large amounts say 2mg (2000mcg) are sometimes used. Injecting GHRH alone is not very effective

Choose a GHRH to add to the GHRP because it will synergisticly amplify the GH pulse.  How few times can I inject for for some better sleep, small anti-aging effect? Just pre-bed     

Step five: Assess tolerance by dosing just once w/ a GHRP pre-bed at half of saturation dose. Then if that goes well go to full saturation dose. If that goes well add a 2nd dosing, If that is fine add a third dosing.


Step six: Decide on a dose. Saturation dose is defined as either 100mcg or 1mcg/kg of bodyweight in the studies

What are GHRP-6, GHRP-2, Ipamorelin, Hexarelin?


In short they are all forms of GHRPs (Growth Hormone Releasing Peptides, Ghrelin-mimetics


Ghrelin is a hunger derived gut-hormone. It is capable of making its way to the pituitary where the GH releasing cells (somatotrophs) reside. Just like GHRH &Somatostatin it also can contact the cell. When it does it reduces Somatostatins effect. Ghrelin increases GH release. It does this in several ways -by encouraging the brain to release more GHRH, amplifying the effect of GHRH when it gets to the somatotroph, benefiting from GHRH being at the cell to amplify Ghrelin's own effect which is in part an increase in GH release and countering Somatostatin's stoppage effect at the cell.

In fact Ghrelin can cause GH release all by itself even if Somatostatin is around. But Ghrelin makes the environment safe forGHRH to act and if GHRH acts when Ghrelin is there the result is what is called a synergistic GH release


modified GRF(1-29). Since it is basically a 30 minute plus lasting GHRH 

What is CJC-1295, CJC-1293, GRF(1-29), Sermorelin and modified GRF(1-29)?


In short they are all forms of GHRH (Growth Hormone Releasing Hormone).

Datrius B. True use either GHRP-2 or Ipamorelin with modified GRF(1-29) I usually rotate around

Somatotrophs are not cells that release prolactin. Prolactin is released by Lactotrophs

injecting GHRH. There will be zero GH release if somatostatin is around and only some if somatostatin is just starting up 

Wake up! GHRPs are the 3rd hormone/peptide that effects GH release. Its presence at the somatotroph causes GH release on its own and with the naturally occurring "on switch" it amplifies GH release. By stopping somatostatin GH is released. Now GHRPs never result in GH bleed. The release they trigger is always a pulse that is over with within 3 hours.

GHRP-6 is sloppier in that it activates a wider array of effects beyond GH release. It causes intense hunger and gastic motility. It can have a mild effect on cortisol and prolactin. It is a first generation GHRP.


GHRP-2 is less sloppy with a more intense GH release, no gastric motility and less hunger effect. It can have an effect within the normal range on prol

catin and cortisol. 2nd gen


Ipamorelin is not sloppy at all. It does not release as much GH as GHRP-2 but it causes virtually no hunger or gastric motility and for the most part does not effect cortisol or prolactin. 3rd gen


You would choose GHRP-2 unless you wanted GHRP-6 for the hunger effect or for the lower release profiles.


You would choose GHRP-2 normally as the most bang for the buck.    Tom's medical grade peptide   authentiquevie@gmail.com

A simple way to look at it - if you can not keep insulin quiet then that time period really won't be a fatloss time period so don't dose the Mod GRF(1-29)/GHRP for lipolysis (i.e. fatty acid liberation) - if you can not be active during that time to burn off the liberated fat then no need to dose the Mod GRF(1-29)/GHRP because fats will just clutter the blood stream and redeposit.

If insulin will be active and you will have a weight workout then consider using Mod GRF(1-29)/GHRP to effect protein metabolism in an anabolic way and to generate intramuscular growth factors for hypertrophy.

Mod GRF(1-29)/GHRP to effect protein metabolism in an anabolic way and to generate intramuscular growth factors for hypertrophy.

Only carbs and fats blunt GH release so avoid these an hour prior to the shot and 15-20 mins post injection


higher level**********Loose the DAC and you lose the albumin. When this happens the remaining compound some GHRH derivative has more attraction for the receptor, stronger binding and because of the pulsation rather then the elevations less molestation of the receptor and more "oh la la!"

Modified GRF(1-29) also known as "CJC1295 w/o DAC and w/o the extra lysine and then terminated properly

I feel I can tell the difference. If it is a cost issue even 25, 40, 50mcg of GHRH will be synergistic

Only carbs and fats blunt GH release so avoid these an hour prior to the shot and 15-20 mins post injection

 growth hormone ligand binds to a receptor and how these events effect the transcription of proteins inside the cell nucleus. We have discussed growth hormone, IGF-1 and insulin in terms of circulatory levels but we have not examined the extent to which these respective ligand-bound receptors interact with one another to effect protein transcription and in particular tissue growth.

Hormonal pulsation is incredibly important. Pulsation conveys hormonal signals which upon ligand receptor-binding transmits information content to regulators of signaling pathways which go on to effect intracellular happenings.

elderly men and women have equally low amplitude GH pulses and reduced IGF-I levels (24, 38). Based on the known properties of GH and IGF-I in vivo, this reduced amplitude, in combination with reduced sex steroid production, likely explains the observed age-dependent change in metabolism, increased fat/lean ratio, decreased muscle strength, reduced exercise tolerance, and increased bone loss. Hence, the functional deficits that result from aging are probably caused by suboptimal signaling from the hypothalamus. An ideal approach for modifying the aging phenotype would be to restore activity of the hypothalamic neurons that control GH pulse amplitude.

GH increases bone density and improves body composition, cognitive function, cardiac function, and exercise tolerance

 In addition to reduced GH release during aging, the concentration of GH receptors in the brain also declines.

GH-deficient children have an increased incidence of anxiety, depression, and attention deficits, which may contribute to their observed learning disabilities in arithmetic, spelling, and reading compared with age-matched controls (202, 204).GH-deficiency in adults is reported to be associated with reduced energy, unfulfilled personal life, low self-esteem, problems controlling emotional reactions, social isolation, impaired social function, mental fatigue, impaired general and mental health, and deficits in cognitive function (205–211). Markedly reduced GH levels, particularly the integrated nocturnal levels, have also been associated with major depressive illness (212). This may explain the increased incidence of depression and poor sleep quality in the elderly population.

Doses of GH that produced supraphysiological levels of IGF-I normalized memory function after 6 months of treatment. Lower doses selected to provide physiological IGF-I concentrations in the blood improved memory function more slowly, but normal function was restored after 12 months of treatment

IGF-I deficiency could be involved in cognitive deficits seen with aging   When they throw in the term "w/o DAC" they are indicating that they are selling D-Ala2 GRF(1-29) + an unstable lysine

Now if you inject GRF(1-29) into the blood streams enzymes will quickly cleave the peptide at the 2nd position. So GRF(1-29) was altered at the 2nd position to prevent this. That alteration was replacing alanine with its isomer D-alanine. D-Ala2 GRF(1-29) binds to the GHRH receptor as well as GHRH does.

Now to make GRF(1-29) even more resilient 3 more amino acids were changed, bringing the total changes to four (tetra - the Greek cardinal number 4). So a tetra subbed GRF(1-29) known as "Modified GRF(1-29)". Modified GRF(1-29) binds to the GHRH receptor as well as GHRH does.


The outcome was consistent with a protective effect of IGF-I on the onset of age-dependent cognitive deficiencies, particularly in speed of information processing

IGF-I was directly related to information processing speed, memory, fluid intelligence, and Mini Mental State Examination score,

Serum IGF-I appears to regulate brain amyloid-B (AB) levels   

Studies on centenarians showed increased prevalence of dementia in those with lowest serum IGF-I levels
  
However, GH treatment produces increases in IGF-I, reverses the age-dependent changes, and increases the number of cortical arterioles


Indeed, chronic administration of a GHRH analog (D-Ala2-GHRH) prevents age-dependent decline in memory in rats (239)


The CNS effects of GH and GHRH are believed to regulate sleep. Slow Wave Sleep and secretion of GH decrease proportionality during aging 


In addition to having stimulatory effects on GH release, GHRH promotes SWS 
bolus
 iv injection
 and intranasal delivery of GHRH increased REM and SWS in old and young human subjects, whereas slow, continuous infusion was ineffective


The GH/ IGF-I axis plays an important role in regulating metabolism, thymic function, bone density, muscle strength, cardiac function, reproductive function, and CNS function (see SectionV). Although rejuvenation of the GH/IGF-I during aging may not have a profound impact on a single function, subtle improvement in all of these important physiological parameters is likely to have a significant impact on quality of life (see Section V). Reduced amplitude of GH pulsatility during aging causes decreases in serum IGF-I levels and is a result of attenuated GHRH signaling

 Chronic activation of the GHS-R by the small molecule agonist MK- 0677 sustained rejuvenation of the GH/IGF-I axis in elderly subjects (25, 38, 277–280). This is accompanied by increased lean body mass and increased bone mass (38, 281–283). In addition to beneficial effects on peripheral tissues, restoring young adult levels of GH and IGF-I is anticipated to be neuroprotective 

n old rats, l-dopa administration restores the amplitude of GH release to that typical of young rats (36), which is reminiscent of the effects of the GHS-R ligand MK-0677 in elderly humans

Perhaps the most exciting recent observation is that ghrelin activation of the GHS-R on T cells antagonizes production of IL-6 (315). This has extraordinary significance to aging because IL-6 levels increase during aging and in diseases common in the elderly, whereas production of the normal counterregulatory hormones, the sex steroids, GH, and IGF-I, decline 

In addition to having negative effects on CNS function, increases in the IL-6/IGF-I ratio is predictive of mortality in frail, elderly women (3, 316, 329, 330). Hence, treating frail elderly subjects chronically with ghrelin mimetics should improve their quality of life and reduce mortality by lowering IL-6 and increasing IGF-I production.

The earliest manifestations of aging are metabolic changes that result in increased fat deposition and reduced muscle mass, which lead to increased likelihood of developing "metabolic disease" (type II diabetes, hyperlipidemia, arteriosclerosis, and hypertension

Although circulating ghrelin concentrations increase between early adulthood and middle age in humans, there is evidence that old age is associated with decreased ghrelin concentrations in rodents and in humans (311, 346). Therefore, enhanced effects of CCK and/or reduced effects of ghrelin may contribute to the development of anorexia and, in some cases, protein malnutrition during aging.

We discussed previously that chronic treatment of elderly subjects with ghrelin mimetics restores the age-related decline in amplitude of GH pulsatility and circulating IGF-I to levels typical of young adults (25, 38, 279). These results suggest that during aging either ghrelin production declines or ghrelin resistance occurs. The orexigenic property of ghrelin coupled with its anabolic effects via the GH/IGF-I axis and its inhibition of the production of inflammatory cytokines (315) indicate that rescue of reduced GHS-R activity 

The lower ghrelin levels in the old subjects were accompanied by increased insulin levels and low serum IGF-I               In rats, leptin administration selectively decreases visceral fat (VF) by approximately 60% and inhibits hepatic glucose production by approximately 80%

relationship between the age-related increase in Visceral Fat and increased insulin resistance may involve the failure of centrally acting leptin to regulate fat distribution

hese results support the conclusion that aged rats are less responsive to leptin because of impaired suppression of hypothalamic NPY synthesis.

leptin resistance accompanies obesity and in most cases insulin resistance. In nonobese animals, both insulin and leptin act on the hypothalamus to inhibit feeding behavior.

this article was derived from the expertise of Datrius B. True 


Stand for health, sitting kills

  • The first area in our body it affects is our brain. When we are physically active, our muscles move and therefore fresh blood and oxygen is pumped through our bodies and delivered to the brain. When this happens, the blow flow triggers many chemicals that our brain releases. Among these are mood chemicals that make us more positive, upbeat, creative and happy. When we sit for a long period of time, these processes slow down which ultimately slows down the rate that our brain is functioning at. This can be experienced as “fogginess” by many people and this state often affects how clearly people think.
  • https://psychneuro.wordpress.com/2015/05/08/think-twice-before-you-sit-down-to-study/
  • DR> Mercola
  • Sitting for extended periods of time is an independent risk factor for poor health and premature death. Even if you are very fit, if you uninterruptedly sit for a great percentage of the time, you’re still at an increased risk of dying prematurely
  • Research by the NASA scientist responsible for monitoring the astronauts, shows your body declines rapidly when sitting for long periods
  • Simply standing up over 30 times a day is a powerful antidote to long periods of sitting and is more effective than walking
  • There are virtually unlimited opportunities for movement throughout the day, from doing housework or gardening, to cooking and even just standing up every 10 minutes
  • It’s not how many hours of sitting that's bad for you; it’s how often you interrupt that sitting that is GOOD for you

Tuesday, December 16, 2014

Alcohol doesn't just kill brain cells....6 Reasons to Stop Drinking Alcohol

1.Alcohol shoot straights to the liver; a direct line shot via the portal vein.  Alcohol is converted to acetaldehyde a volatile terror which attaches to DNA, which forms a myriad of cancer causing chemicals and halts the methylation process. 

2.Acetaldehyde leeches onto  the backbone of cells, hemoglobin, serotonin and dopamine.   

3.For the liver to process acetaldehyde it requires so much oxygen, that other metabolic process fail for lack of oxygen, suffocating living cells and creating toxic pathogens.  

4.High levels of alcohol impede the wound heal process damaging vital organs.

5.Even moderate alcohol use on a chronic level, kills the metabolism of fatty acids , leading to fatty liver. 

6.Alcohol stops the secretion of vasopressin (anti-diuretic, alertness neurohormone) making you urinate.