16 replies to this topic

[David Savage]

So...

 

For the New Year, like many others, I have committed to ya know, getting in better shape.

 

Nope, not the first round for me and certainly not the first round by the change of the year, but HERE WE GO AGAIN!

 

A couple of years ago, after healing myself from some gastrointestinal issues, I heard that I was going to be a Grandfather! 

 

Wow, was I excited.

 

I had the opportunity, after really not wanting longevity, to have some time with a grandchild.  Exciting times!

 

If you would have told me, years ago, that by taking a pill would increase my life 10 years, I would've told you to "Fuck Right OFF, and Keep going".  

 

My health was shit!

 

Body is broken down.

Fat around the belly(overall chubby).

Barely could get out of bed.

Could hardly work...

 

Got over that, will explain more as I go (probably).

 

Anyways, in better health, but still a lot overweight, case of beer and a pack a day smoker, learning of my new grandchild, I knew it was time to get my shit together!  

 

Set a quit day on the darts, started to taper of the suds and was thinking by the time the baby was born, all would be in order.

 

WRONG!

 

Didn't manage to start throttling back on the weight until Mid 2017 and didn't end of quitting the darts until August...

 

All good though!

 

In 2 months, starting with a CR+ Velocity protocol, I lost 50 Pounds!!

(Protein shakes and IF ->approx 600-800 calories per day)

By the time I quit smoking, I was 1000% better than had been only a few months prior.

Tapered off the beer, eating KETO-LCHF and kept on keeping on!!

 

Well, through the balance of summer and into the fall, old habits snuck up.  I mean really, who doesn't want to hang out outside with a cold one when the sun is bright and the weather is hot?  

 

Was still quitting smoking (Swapped the cigs for a Vape), and was all good.  Eeeked outside of the lines, but given the fact that I had dropped 20% of my bodyweight, I had a lot of wiggle room.

 

Through my fasting period, I had lost a couple of very close family members.  My stepmother and stepfather...fortunately, I still have a couple of spares in that department, but with a regular work routine, hospital stays and funeral plans, I guess I just got overwhelmed and when came time to take a break, I completely shut down!

 

Shit built up and may have been one of the factors that lead to my work contract being terminated in November.

 

FUUUUUUUUUUUUUUUCK!

 

Well, November was a wash!

 

Tried to keep to most of my diet, but had a lot of brewskies to tie down the month...this lead into similar patterns in the beginning of December and by mid-month, I realized it was time to shake this shit off and get back to the program!

 

Not really the best time...but I was going to giver a whirl!

 

My first Velocity fast lasted 3 days on a 4-day plan...not bad.  Seriously, if you can go 3 days on maintenance macros of proteins by shakes alone, it's not a terrible thang.  The intent was to be able to do a 5-day water fast by Christmas.

 

Yeah-Fucking-Right!

 

No way that was in the cards.  Between kids, granddaughter, family and friends, we ate and drank like the turn of this year would be our last...but all the while, I kept my 5 day water fast in the back of my head thinking that this would be my launch into 2018!

 

January 1st...had the kids and friends over for a traditional brunch - I did most of the cooking - followed up by a large dinner and then...I began!

 

Well, fuck me FREDDY!

 

I had kind of figured that carb loading into a fast was a bad idea, but by the end of January 2nd, I would have cut you for a packet of ketchup!

 

There was some physical activity for the first 3 days, weights and cardio.  Idea being that I wanted to hop into a Keto diet after the fast and what better way to get into ketogensis than to fast through the glucose depletion stage.  Worked well and I would surmise that by the 3rd, I was pissing ketones!

 

Sure, I could have used the strips to check, but all honesty, who cares?

 

My weight starting January 2 was 188 by the time I quit my fast - Day 4 - was 176 and I felt like a fucking king!

 

I stopped due to a going away party for my son and his friends.  He and one of his mates, shipping back to Base (Canadian Forces), the others heading in seperate directions from the UK to other remote areas of Canada, some only a few blocks away, but we all knew that it would be months before we would re-unite and really, I just couldn't miss the opportunity to say my "Good-byes".

 

My Break Fast - started with a couple of Bick's Pickles.  Holy fuck!! BEST PICKLES I EVER ATE!!

 

And followed up with a couple of lettuce wrapped - Freshly Grounded - Sous Vide Cooked and BBQ crisped Burgers.  Mmmmmmmmmmm....

 

Did that before hitting the bar to meet the kids, sipped a diet Pepsi while I was there - in spite of spending a couple hundred on snack menu items for the kids - and hit the sheets by 1:00am(ish).

 

I've been going strong and knew that my weight loss from the fast would bounce back on water weight alone, but over the last couple of weeks, I've managed to keep to a '1-meal/day' IF program - LC - and shuck off to 174LBS.  (Have had last weekend with beer n wings, this weekend have already strapped on a case, will be bright at it come Monday).

 

So...TL;DR

 

The FAST!!

 

I have a monumental birthday in February...I only actually realize it's monumental because I have to renew my license...but given my gains on losses, wanted to see if I could SEAL the DEAL by one last fast in February!

 

Starting...I am already Keto and according to xEva, this is probably a good place to start, razors off 2-3 days from a full fast.

 

Going into the end of month, I plan to keep on a 1-meal/day IF-LC, shedding some weight and adapting to a fasting protocol and will keep my sups up to the February 1st.

 

AM:

Omega 3 - 2300mg.

Pine Bark Extract - 750mg.

Hyaluronic Acid - 750mg.

Mucuna Puriens - 750mg.

Milk Thistle - 750mg.

Lysine - 1000mg.

1 TBSP Coconut oil.

1 TBSP Butter.

 

Afternoon:

Hyaluronic Acid - 750mg.

 

Evening:

Hyaluronic Acid - 750mg.

Berberine + Milk Thistle -375MG/ea - total 750mg cap.

Lysine - 1000mg.

Vitamin C - 1000mg.

Niacin - 1500mg.

 

(PBE, HA, MP, MT, N are approximated - self-capped - size 00)

 

The protocol is just a combination of what I believe will give me, well, the best chances of being more handsome on the backside of this adventure.

 

Minimum Fast - 4 days.  Maximum - 9 days.

Birthday is on the 11th and I want to break my fast easy before getting completely SHITFACED!

 

 

Will be updating as I continue...

 

Feel free to chime in with questions and suggestions.

 

I've learned a lot from Turnbuckle, xEva, aconita and Nate...few others...look forward to hearing what you may have to add.

Edited by David Savage, 20 January 2018 - 04:48 AM.

[David Savage]

One Meal/Day!!

 

Several years ago - as a field based technician and running 2 of my own businesses, I wasn't feeling altogether great.

 

Having kids, my wife told me to go to her doctor for a check up...

 

Since Highskewl, I had suffered from Migraine Headaches, took handfuls of Tylenol and given what I had been previously prescribed, what I was doing was as effective with seemingly fewer side effects and was a boatload cheaper than the scripts.

 

In HS - I had seen many a Quack - all quick with the script pad and another 2-week followup.

At my turn-point, I was on over $300/wk of chemicals that had built based on each adding another symptom that the following would eliminate.

 

Started off with a headache added a script; lead to tummy troubles added a script; lead to insomnia added a script; lead to anxieties added a script...

 

FUCK!

 

What the fuck were they doing to me?

 

I started off with a headache and after $300/mo, not being able to sleep, being sick all the time and gaining a chronic shake in my left hand, not being able to sit in a room with a single person - I got more Headaches!!

 

FULL FUCKING CIRCLE!

 

Enter Tylenol...

 

Really, back then, it was just Tylenol.  Not a chemical that killed your liver and if taken with alcohol could kill you...was cheap, OTC and worked a fuck pile better than what the pros were subbing.

 

Anything is good in moderation, including moderation!

 

I was really outside of moderation by the time I went to the doc, told her about my usage and my diet and she said that my liver enzymes showed signs of issues and that my diet was surely going to fast track me to diabetes!

 

FUCK!!

 

My wife's mother had died of diabetes (1) and with us being young with 2 kids, she wasn't wanting to see me do any harm to myself and to start taking the docs advice.

 

Seemed logical.

 

My diet - given that I worked 7 days/wk, only afforded me 1 meal per day - (Can you see where this is going?)

 

That's right...If I would have kept to my original diet - 1 Meal Per Day - which in effect is the same IF I am on currently - and switched to ADVIL - I most probably wouldn't be at this forum, wouldn't have gained 50% extra on the beltline, wouldn't have had my physical issues...

 

For all intents and purposes, I was in great shape.  Spent 8-10 hours on a ladder and was physically active, just didn't rely on trying to force myself to eat convenient foods, because even then, they were inconvenient.

 

[/facepalm]

 

Okay...I wasn't always having the best 1 meal per day, had no fucking clue what keto or LC was, and didn't focus on it.

Why?

Didn't need to.  Still, really don't need to...If I were more patient (thanks to the internet, who really is?), I wouldn't even give a shit what my 1-meal/day is now.

 

Whatever...

 

Anyways...

 

As I have floated through a lot of the Keto/Paleo/IF threads/youtube vids, the same things always seem to come up - what do you eat?

 

Well...some of the shit that these people eat, I wouldn't feed to my dog!!

 

No fucking wonder they FAIL!

 

To me, a lot of diet plans - and no offense meant to members here - seems like you are looking to dare others into trying shit just for the sake of trying shit and justifying it in the name of 'Greater Good'

 

Like that fucking dipstick - Sensei.

 

Dude got his own thread, slurping back OO and his C60 and we can only speculate on proof of 2 maybe 3 things - you pick

1.  C60oo - May not actually do anything - given what he has consumed to his returns = ZILCH.

2.  C60oo - Adding more upon more to your daily diet, certainly doesn't amp up the effectiveness of it. Equation ->0+0=0

3.  That early settler mated with buffalo. 

 

Seriously, after a week of his dosing on that much oo, I can only imagine his toilet resembles that of a [Insert Random Truck Stop HERE], after an 'All you can Eat Chilli luncheon'. 

 

What's the fucking point???

He has to be daring somebody to either try and match or beat him...no point otherwise.

 

[/digression]

 

Anyways...TL;DR

 

One Meal/day - Back where I started years ago - will continue this into my fast as this should:

1.  Keep me in Ketosis.

2.  Ready my body for additional Calorie Restriction.

3.  Keep me Fat Adapted - running on Ketones.

4.  Add in the benefits of weight loss.

 

LC Diet - 1 Meal/Day

 

Sample Meals:

Carne Asada

 asada.JPG   107.07KB   0 downloads

Chicken Lettuce Wraps

 chicken lettuce.JPG   121.23KB   0 downloads

Tenderloin and Tilapia - Side of Mashed Cauliflower

 surfnturf.JPG   111.58KB   0 downloads

Prime Rib Roast

 pr.JPG   107.04KB   0 downloads

 

 

Recipes for succes with LC/Keto/IF!

Edited by David Savage, 20 January 2018 - 05:54 AM.

[David Savage]

Thread Title = Niacin and Water Fasting for Vanity.

 

Why?

 

Great question!!

 

Has it been tried?

 

Not that I've seen...but really, this is not the reason.

 

I mean, if I wanted to try fasting and something that hasn't been tried, I probably could have posted 'Eating Toe Jam and Water Fasting'...but I really have no idea if eating Toe Jam would promote or enhance autophagy.  Not that I am actually sure that this will have any impact on autophagy, but again, as this is a thread for VANITY, does it matter?

 

Probably not!!

 

But I haven't yet seen anybody post a single thread stating that Toe Jam Consumption might make you more handsome...maybe this is something Sensei could try for the house??

 

NIACIN!!

 

I fucking love this stuff!

 

After figuring out how to get rid of the Flush with regular B3, it is one of the actual supplements that you can feel active.

 

No...dammit...not just the flush, there's other stuffs too!!

 

 

 

Nobody seems to understand very well how niacin works. This leads to some confusion. Many people think that niacin inhibits the production of VLDL, free fatty acids, and ketones; preventing the use of fat as an energy source. And it does!

So it makes you fat, right?

No, because these effects are temporary, and are followed, often after 3 to 5 hours, by a large increase in circulating growth hormone, cortisol and glucagon. These hormones are associated with (maybe they cause, maybe are caused by) a large increase in free fatty acids and ketones in circulation, but not with an increase in VLDL secretion by the liver. So ketosis is at first inhibited by niacin, and then comes in full force after a few hours.

LINK

 

Pretty Kewl, right?

 

No?

 

Not getting it, hey?

 

I get it...I had an issue resolving this when I added Niacin to my IF days as well.

 

First, let's start with how the fuck do you get rid of the Niacin Flush??

 

This...is a lot easier than you would suspect.  For anybody who takes Niacin once per day, in any dose, the Flush is pretty much inevitable until your body is used to it.  If you take it in smaller doses, multiple times per day - your adjustment period can be reduced to a single day?

 

What???

 

Yup...

 

Here's how I have and have coached others to beat the flush!

 

Day 1 - After your last meal of the day - take a Dose of Niacin.  Because I cap my own, mine are approx - 750mg/dose give-or-take...

Drop one of them motherfuckers and get ready for a COLD SHOWER because all hell is about to break loose!

 

Day 2 - Upon waking - Take the SAME DOSE - Flush is reduced to a prickly warm sensation.

Day 2 - At lunch - eating or not - Take the SAME DOSE - you will feel it, but no flush...

Day 2 - After last meal - Take the SAME DOSE - you probably won't even know you've taken one...

 

That's it!!

 

You are FLUSH ADAPTED!!

 

w00t!

 

Now...here's the issue with taking Niacin in this same protocol if you are Keto/Fat Adapted...

 

Let's say, you are taking a road trip on an endless highway in an electric car.  You decide to charge the battery and while it's charging - 3 to 5 hours - it will still go, but really fucking slowly. Bzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz

 

If you are Fat Adapted and you take something that cuts off your fats and ketones for 3-5 hours, you feel like a bag of shit, have zero energy and your body is CRAVING FOOD!

 

So, seriously...why the fuck would I do this on a Water Fast??

 

Another Great Question and let me explain!

 

Over the last couple weeks, I've gone through this same very feeling - Bzzz and Hungry!!!  If your plan is to not eat throughout the day, this is troublesome...so I bro-scienced logic in that if I want this to potentially break down more fat and give me a surge of ketones, the best time to do this is while I'm Sleeping. Guess what??

 

It actually works.

 

If I take a Double Dose of Niacin in the evening, I keep Flush Adapted and have ample energy throughout the following day.

 

Added Benefits:

This, actually gives me a deeper sleep and helps to re-tune the clock...being unemployed n all, easy to fall into a rhythm of up all night and sleep all day...but the wife gets justifiably a little cranky when I do this, plus I take days babysitting the Granddaughter and it requires a lot of energy as my ketones seem to keep me throughout the day - until my meal. 

 

During a Water Fast:

I again bro-science my logic into thinking that it may just do the same for a water fast and losing that spare tire that is reluctant to reduce throughout my 2018 mission (being more Handsome).

 

There is more to the story in a sciencey link I posted for Nate with the whole NAD+ thang, but again, this is for VANITY...fuck the sciency stuff!

LINK

 

Maybe it helps out with Longevity...Maybe I have to quit because it zaps my energy...until I try, I just won't know...

 

 

Edited by David Savage, 20 January 2018 - 06:53 AM.

[David Savage]

Niacin Fun Fact!

 

If you go through the 24-hour dosing protocol for Niacin adaptation as posted previously, this can actually be counteracted by alcohol consumption.

 

Alcohol brings back the flush!!

 

In saying this...and please learn from my experience last night...DO NOT, throw back a few beers, dermaroll your face and chase this with 1500mg of B3  - Unless you are some sort of sadomasochist, in which case - Go Ahead! (Not judging)

 

Holy fuckity fuck!

 

I thought I was going to have to start peeling my skin off!

 

So, just kind of pondering here...

 

If we can hyper dose on Niacin to beat the flushing, does that mean when we do consume alcohol or go prolonged periods of time without large doses of Niacin that we are deficient?

 

Like, is flushing our body's way of saying...you're not there yet?

Edited by David Savage, 20 January 2018 - 04:39 PM.

[David Savage]

Well, FUCK...

 

All I wanted to do was look more handsome...turns out, this might just add to Longevity too???

 

Not wanting to get all sciency, but this does add a little more motivation into my fasting protocol - Niacin and Water Fasting.

 

 

Front Mol Neurosci. 2017; 10: 377.

Published online 2017 November 14. doi:  10.3389/fnmol.2017.00377

PMCID: PMC5694488

Ketone-Based Metabolic Therapy: Is Increased NAD+ a Primary Mechanism?

Marwa Elamin,1 David N. Ruskin,2 Susan A. Masino,2,* and Paola Sacchetti1,*

Author information ► Article notes ► Copyright and License information ►

 

Go to:

Abstract

The ketogenic diet’s (KD) anticonvulsant effects have been well-documented for nearly a century, including in randomized controlled trials. Some patients become seizure-free and some remain so after diet cessation. Many recent studies have explored its expanded therapeutic potential in diverse neurological disorders, yet no mechanism(s) of action have been established. The diet’s high fat, low carbohydrate composition reduces glucose utilization and promotes the production of ketone bodies. Ketone bodies are a more efficient energy source than glucose and improve mitochondrial function and biogenesis. Cellular energy production depends on the metabolic coenzyme nicotinamide adenine dinucleotide (NAD), a marker for mitochondrial and cellular health. Furthermore, NAD activates downstream signaling pathways (such as the sirtuin enzymes) associated with major benefits such as longevity and reduced inflammation; thus, increasing NAD is a coveted therapeutic endpoint. Based on differential NAD+ utilization during glucose- vs. ketone body-based acetyl-CoA generation for entry into the tricarboxylic cycle, we propose that a KD will increase the NAD+/NADH ratio. When rats were fed ad libitum KD, significant increases in hippocampal NAD+/NADH ratio and blood ketone bodies were detected already at 2 days and remained elevated at 3 weeks, indicating an early and persistent metabolic shift. Based on diverse published literature and these initial data we suggest that increased NAD during ketolytic metabolism may be a primary mechanism behind the beneficial effects of this metabolic therapy in a variety of brain disorders and in promoting health and longevity.

Keywords: ketone bodies, metabolism, hippocampus, epilepsy, neurodegeneration, Alzheimer’s disease, nicotinamide adenine dinucleotide, longevity

Go to:

Introduction: Ketogenic Diet and Disorders of The Nervous System

A diet high in fat, low in carbohydrate and sufficient in protein will automatically shift the dependency of energy production in the body from primarily glucose to primarily ketone bodies and is termed a “ketogenic diet” (KD; Branco et al., 2016; Masino, 2017). This dietary approach was developed nearly 100 years ago as metabolic therapy to mimic the metabolic changes that occur during fasting after observing that upon halting food intake, seizures would stop in epileptic people. The KD is well-established as a treatment for epileptic seizures and variations of the diet can be used in children and adults and can be more effective than medication in stopping seizures (Pulford, 1927; Neal et al., 2008). The KD can also prevent seizure progression (epileptogenesis) in animal models and patients (Muller-Schwarze et al., 1999; Neal et al., 2008; Lusardi et al., 2015). Some patients become seizure-free, and remain so even after diet cessation (Martinez et al., 2007; Patel et al., 2010; Caraballo et al., 2011). These lasting outcomes are likely to rely on epigenetic changes (Boison, 2017).

Metabolic dysfunction is increasingly appreciated as a fundamental pathology across disease states (Zhu and Chu, 2010; García-Escudero et al., 2013; Pathak et al., 2013). In models of neurodegenerative diseases, metabolic therapy with a KD or analogous ketone-enhancing metabolic strategies have beneficial effects in cultured neurons, animal models, and in patients. The ketone body β-hydroxybutyrate (β-OHB) protected cultured dopaminergic substantia nigra cells from N-methyl-4-phenylpyridinium (MPP+) toxicity and hippocampal neurons from amyloid β toxicity (Kashiwaya et al., 2000), and improved the disease rating score in Parkinsonian patients (Vanitallie et al., 2005). In vivo and in vitro administration of ketone esters reduced histological and biochemical pathologies and improved cognition, anxiety and motor performance in mouse models of Alzheimer’s disease (Liu et al., 2011; Hui et al., 2012; Brownlow et al., 2013; Kashiwaya et al., 2013; Zhang et al., 2013; Pawlosky et al., 2017). KD improved memory of patients with mild cognitive impairment (Krikorian et al., 2012), and administration of a ketone ester or medium chain triglycerides (often a component of ketogenic treatment) enhanced memory and cognition in Alzheimer’s patients (Reger et al., 2004; Newport et al., 2015; Cunnane et al., 2016). Treatment with a KD suppressed inflammation and improved motor disabilities in a multiple sclerosis model (Kim et al., 2012), altered disease progression and improved motor performance and neuronal survival in an amyotrophic lateral sclerosis model (Zhao et al., 2006), decreased the expression of apoptotic mediators in a traumatic brain injury model (Hu et al., 2009), and improved motor outcomes in a spinal cord injury model (Streijger et al., 2013).

It is becoming apparent that beneficial effects of ketogenic therapy extend beyond epilepsy, neurodegenerative disorders, and brain/spinal cord injury. The KD is broadly effective in improving core behavioral symptoms in animal models of autism spectrum disorder (Ruskin et al., 2013b, 2017a,b; Ahn et al., 2014; Verpeut et al., 2016; Castro et al., 2017; Dai et al., 2017), and in autistic patients (Evangeliou et al., 2003; Masino et al., 2011b; Spilioti et al., 2013). The KD is receiving growing interest in oncology as tumors are highly glucose-dependent (the Warburg effect; Seyfried and Mukherjee, 2005; Zuccoli et al., 2010; Schmidt et al., 2011; Klement et al., 2016; Lussier et al., 2016; Khodadadi et al., 2017). Also, due to the high efficiency of metabolizing fat when carbohydrates are minimal (Forsythe et al., 2010), the KD has been promoted for weight reduction (Jenkins et al., 2009; Partsalaki et al., 2012; Paoli, 2014; Gomez-Arbelaez et al., 2017) and for treatment or reversal of type II diabetes and metabolic syndrome (Yancy et al., 2005; Volek et al., 2008, 2009; Westman et al., 2008; Hussain et al., 2012; Tay et al., 2015; McKenzie et al., 2017).

In addition, healthy, disease-free cells and animals can also benefit from this therapy. The use of ketone bodies as an energy source appears to be associated with a healthier metabolic phenotype that renders cells more resistant to external insults. Ketogenic treatment decreased myocardial damage after ischemic injury, reduced lung injury after hemorrhagic shock, enhanced kidney resistance to oxidative stress, and protected neurons against glutamate-induced toxicity (Zou et al., 2002; Koustova et al., 2003; Noh et al., 2006; Shimazu et al., 2013). At the cognitive level, beneficial effects on learning and memory were reported (Brownlow et al., 2017; Newman et al., 2017). KD in mice started at 8 weeks of age did not affect longevity (Douris et al., 2015); however, KD started midlife extends longevity and healthspan (Newman et al., 2017; Roberts et al., 2017).

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Mechanisms of Ketogenic Therapy: Evidence for Increased NAD+

Many mechanisms have been proposed to explain the anti-seizure and neuroprotective effects of the diet, such as enhanced mitochondrial biogenesis (Bough et al., 2006), decreased formation of reactive oxygen radicals (Sullivan et al., 2004), altered transmitter levels and ion channel function (Schwartzkroin, 1999; Bough and Rho, 2007), increased adenosine (Masino et al., 2011a; Masino and Rho, 2012), and decreased DNA methylation (Kobow et al., 2013; Lusardi et al., 2015). Each one of these mechanisms could account for some of the beneficial effects of the ketogenic therapy. However, to date fundamental metabolic mechanism(s) which could explain diverse beneficial effects across numerous diseases have yet to be confirmed. If uncovered, such mechanism(s) could provide a fundamental answer to “how does the KD work?”—a lingering question and a topic of intense resurgent research efforts and clinical interest. A unifying mechanism of action could also serve as a target for the development of therapeutics that enhance cellular and metabolic health and provide the metabolic resilience necessary to prevent and combat neurological diseases.

Glucose and ketone bodies are used to provide energy in the form of ATP. Many tissues in the body—such as muscle tissues—can oxidize fatty acids to produce energy. As one exception, in the central nervous system ketolysis is expected to be the primary pathway of energy production: neurons and oligodendrocytes have a limited capacity for mitochondrial fatty acid β oxidation (Edmond, 1992; Achanta and Rae, 2017). The ketone bodies acetoacetate (AcAc) and β-OHB are therefore the main energy source in the brain during ketosis, and the metabolism of glucose versus ketone bodies results in a differential reduction rate of nicotinamide adenine dinucleotide (NAD), an essential metabolic coenzyme and signaling molecule. NAD exists in oxidized and reduced forms, NAD+ and NADH, respectively, and whereas both glucose and ketone pathways each produce two molecules of acetyl-CoA, glucose reduces four molecules of NAD+ and ketone bodies reduce either one (β-OHB), or none (AcAc) during acetyl-CoA synthesis (Lodish et al., 2000; Cotter et al., 2013; Figure  Figure1).1). A decreased reduction of NAD+ in the brain would be expected to result in increased NAD+/NADH ratio, with more oxidized molecules available for bioenergetic demands.

Figure 1

Schematic of NAD+ consumption during metabolism of glucose vs. ketone bodies. Both glucose and ketone bodies lead to the formation of two molecules of acetyl-CoA which subsequently enter the citric acid cycle and participate in energy production. Although ...

Increasing the NAD+/NADH ratio has multiple important implications: improved bioavailability of NAD+ molecules has been linked to anti-aging (Scheibye-Knudsen et al., 2014), longevity (van der Veer et al., 2007; Zhang et al., 2016) and other potentially beneficial effects. For example, an increased NAD+/NADH ratio was found to enhance mitochondrial function and protect against oxidative stress, and diverse research has shown that NAD molecules play an important role in cellular respiration, mitochondrial biogenesis and redox reactions (Yang and Sauve, 2016). NAD+ also serves as substrate for enzymes affecting cellular functions ranging from gene expression to post-translational protein modifications, such as deacetylation and ADP-ribosylation (Belenky et al., 2007).

We propose that the decreased reduction rate of NAD+ to NADH during ketone-based metabolism increases availability of NAD+ and thus alters the NAD+/NADH ratio. This would occur during sufficient exogenous ketone administration or during fasting or adhering to a KD, i.e., when ketones are used as a main source of energy. Considering the pivotal role of NAD+ in cellular health, and that differential NAD reduction is inherent in this metabolic pathway, we suggest that this differential rate of NAD+ reduction (and thus an increase in NAD+ availability) is a primary mechanism of ketogenic therapy: increased NAD+ can potentially be the starting point for many of the diverse benefits of this metabolic treatment.

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Ketogenic Diet-Induced Increase in Brain NAD+/NADH Ratio Is Rapid, Persistent and Region Specific

As an initial test of this hypothesis, we quantified and compared KD-induced changes in blood ketones and in NAD+/NADH ratio in hippocampus and cerebral cortex of normal adult rats. Sprague-Dawley male rats (Trinity College, age 9–14 weeks, n = 20) were fed ad libitum either a standard chow diet (CD; Purina 5001; PharmaServ, Framingham, MA, USA), or a 6:1 [fat: (protein + carbohydrates); #F3666; Bio-Serv, Frenchtown, NJ, USA] KD for 2 days or 3 weeks. Analysis of trunk serum collected showed that a KD induced a significant increase in ketone bodies (β-OHB; the primary circulating ketone body; Figure  Figure2A),2A), consistent with previous experimental and clinical work (Nabbout et al., 2010; Ruskin et al., 2013a).

Figure 2

Changes in blood ketones and brain nicotinamide adenine dinucleotide (NAD) after ketogenic diet (KD) treatment. (A)Blood levels of β-hydroxybutyrate (β-OHB; mmol/L) after 2 days (2d KD; n = 3) and 3 weeks (3w KD; n = 4) of KD treatment ...

To begin to evaluate if, when and where alterations in NAD occurred in brain during ketone-based metabolism we performed NAD analysis on two regions, hippocampus and frontal cortex, after either a 2 days or a 3 weeks KD treatment. Three weeks exposure has been demonstrated to impact behavior and neuronal excitability in diverse paradigms (Hori et al., 1997; Cullingford et al., 2002; Ruskin et al., 2009; Masino et al., 2011a). As demonstrated by ketone body levels (Figure  (Figure2A),2A), metabolic changes were significant within 2 days.

Twenty milligram samples of tissue from each region were homogenized in NAD extraction buffer, centrifuged and deproteinized using 10 kDa molecular cut-off filters. Analysis of NAD was performed using an enzymatic NAD+/NADH quantification kit (Sigma Aldrich, St. Louis, MO, USA) according to manufacturer’s instructions. Fractions of samples were incubated for 5 min at room temperature for the detection of total NAD (tNAD), while equal amounts were heated to 60°C for 30 min to decompose NAD+ and leave unaltered NADH. tNAD and NADH were quantified with a colorimetric measure. Values of NADH were subtracted from tNAD to calculate the amount of NAD+ present in the samples.

After 3 weeks of treatment, extracted hippocampi showed a significant increase in NAD+/NADH ratio in the KD-fed group compared to the CD-fed group (Figure  (Figure2B).2B). Interestingly, no detectable changes in NAD+/NADH ratios were observed in frontal cortices of the same animals (Figure  (Figure2C2C).

Interestingly, a robust and similar increase in NAD+/NADH ratio was already detectable in hippocampi after 2 days of KD treatment (Figure  (Figure2D).2D). This result aligns with previous work (Nabbout et al., 2010; Ruskin et al., 2013a) showing that metabolic changes are present within 2 days and further corroborates the evidence that ketone bodies increase NAD+ availability rapidly. Increases in NAD+/NADH ratios were due to increases in NAD+ as NADH levels were not changed significantly by diet treatments (CD: 3.25 ± 0.32 pmol/μg proteins; 2 days: 2.58 ± 0.21; 3 weeks: 2.68 ± 0.21; not significant). The changes quantified in the hippocampus are consistent with the predicted metabolic consumption, as highlighted in the metabolic pathways (Figure  (Figure11).

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Perspective and Implications

Consistent with our predictions we found clear evidence that metabolic therapy with a KD increases NAD+/NADH, a mechanism that could compensate for metabolic dysregulation and serve as a common start-point for the diverse beneficial metabolic and mitochondrial effects obtained with ketogenic treatments (Bough and Rho, 2007; Masino and Geiger, 2008). As noted above, a comparison of the metabolic pathways of glucose and ketone bodies (Figure  (Figure1)1) suggests that the use of ketone bodies as main energy fuel requires fewer NAD+ molecules than glucose (by a factor of 4), which should lead to an increased cellular availability of this vital coenzyme. Interestingly, β-OHB or a ketone ester precursor show protective effects by counterbalancing the decrease in NAD+/NADH ratio in cases of neurotoxicity (Maalouf et al., 2007; Zhang et al., 2013), confirming the ability of β-OHB to modulate NAD+/NADH levels. Ketone ester treatment oxidizes the cytoplasmic NAD+/NADH couple in hippocampus and cortex in aged, affected Alzheimer’s disease model mice, and reverses an apparent overoxidation of the mitochondrial couple in the hippocampus (Pawlosky et al., 2017). Thus this study and our study of the whole-cell couple suggest clear positive metabolic effects of ketolytic metabolism.

In general, the hippocampus has been described as a seizure gate (Heinemann et al., 1992) and it is one of the first brain regions to be affected in Alzheimer’s type dementia; cortical changes appear later in the disease (Braak and Braak, 1998). Unexpectedly, our data show that a KD increased NAD+/NADH in the hippocampus but not in the cerebral cortex, indicating regional specificity at the time points sampled. It is possible that changes mobilized by a KD could be more rapid or pronounced in more metabolically active brain regions: the hippocampus displays a higher metabolic rate than the cerebral cortex (Feng et al., 1988). Related to this, an early decrease in metabolic rate of glucose in the hippocampus, but not in cerebral cortex, was detected in patients who received a postmortem diagnosis of Alzheimer’s disease (Mosconi et al., 2009). Because of its high metabolic rate and increased vulnerability to hypoxia, oxidative stress, and metabolic dysfunction, the hippocampus could benefit more—or more rapidly—than other regions from KD-induced metabolic changes, including increased NAD+ levels.

Rapid increases in NAD+/NADH ratio could partially explain the ability of a KD to stop seizures in many patients within a few days of KD treatment (Freeman and Vining, 1999). For example, NAD+and NADH molecules can modulate directly the opening of ion channels important for neuronal excitability, such as ATP-sensitive and voltage-gated potassium channels (Dukes et al., 1994; Tipparaju et al., 2005). Accordingly, a rapid decrease in NAD+ availability and consequent effect on neuronal excitability should be expected upon discontinuation of treatment. Interestingly, 15% of refractory epileptic patients experienced a rapid recurrence of seizures after KD discontinuation (Martinez et al., 2007); others remain seizure-free. The differential response among patients to treatment cessation indicates the existence of multiple downstream mechanisms and epigenetic changes (Masino and Rho, 2012; Lusardi et al., 2015) implicated in seizure control. Upregulation of key ketogenic enzymes, mainly mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase, after longer periods of ketogenic treatment (Cullingford et al., 2002) might also play a role in the maintenance of the beneficial effects even after discontinuation of the diet. More work is needed on downstream and lasting effects of metabolic therapy.

Consistent with these reported effects, previous work showed that addition of ketone bodies also prevented the expected decrease in NAD+/NADH ratio induced by toxic doses of calcium and in parallel decreased the production of reactive oxygen species (ROS), a major source of cellular oxidative stress (Maalouf et al., 2007); oxidative stress is detrimental and linked to neuronal death and neurodegenerative diseases (Naoi et al., 2005). Altering the NAD+/NADH ratio can control the rate of ROS production (Kussmaul and Hirst, 2006) and impact downstream enzymatic levels and activities that regulate apoptosis and inflammation (Yeung et al., 2004; Chen et al., 2008; Zhu et al., 2011). Enhanced NAD+/NADH should thus decrease inflammation, an effect observed in KD treatment (Forsythe et al., 2008; Ruskin et al., 2009; Yang and Cheng, 2010; Dupuis et al., 2015; Nandivada et al., 2016). Overall, increasing the NAD+/NADH ratio through a number of ketone-enhancing treatments should protect against oxidative stress and enhance mitochondrial and cellular health.

Regarding gene expression, consuming a KD has been found to impact expression patterns of genes modulating neuroinflammation, proliferation, and apoptosis such as cyclooxygenase, tumor necrosis factor-α, and insulin-like growth factor 1 (Cheng et al., 2003; Jeong et al., 2011). Although increased NAD+ cannot exert these effects directly, NAD+ can impact gene expression through the action of sirtuin enzymes. Increasing NAD+ availability or the NAD+/NADH ratio can increase the activity of the NAD-dependent SIRT1 enzyme (the most abundant member of the sirtuin family; Landry et al., 2000; Chen et al., 2008). The main function of SIRT1 is deacetylation of targets that regulate apoptosis and transcription factors such as peroxisome proliferator-activated receptor-γ and the tumor suppressor protein p53 (Yeung et al., 2004; Zhu et al., 2011). Hence, some of the expected downstream consequences of increasing NAD+ with ketogenic treatment are decreased cell death, inhibition of inflammation, and modulation of gene expression and epigenetic changes through activation of sirtuin enzymes (Janke et al., 2015).

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Conclusion

Here we outline the overall implications and evidence for a rapid and region-specific change in NAD+/NADH as a direct result of consuming a KD. We hypothesize this as a new and fundamental addition to potential key mechanisms underlying beneficial antiseizure, neuroprotective and disease-modifying effects of KD. Because NAD+ can modulate ion channels, enhance mitochondrial health, decrease oxidative stress, and impact gene expression, an increase in NAD+ and/or NAD+/NADH ratio is a mechanism that can account for several diverse (and seemingly-unrelated) effects of ketogenic therapy. Furthermore, benefits of increasing NAD+ such as life-span extension and enhancing cellular health have long been documented (Lin et al., 2000), and pharmaceutical companies are currently manufacturing and selling supplements that contain NAD+ precursors such as nicotinamide or nicotinamide riboside in an attempt to increase endogenous NAD+ levels and enhance metabolic resilience—an outcome that may also be achieved physiologically by ketogenic strategies.

At this time more research is needed to further identify where and when ketogenic therapy increases the NAD+/NADH ratio, and to delineate specific downstream effects. It is also important to ascertain if changes in the NAD+/NADH ratio are caused by changes in NAD+ or NADH, as levels of these two redox molecules can also vary independently (Wilhelm and Hirrlinger, 2011). Regardless, diverse lines of evidence place NAD+ at the center of metabolic health and disease, and evidence from our work and others supports the hypothesis that increased NAD+ is a fundamental molecular mechanism of the KD. Our findings also indicate the potential for a greater role for this metabolic therapy in areas with high metabolic demand and vulnerability to environmental insults and oxidative stress such as the hippocampus. Taken together, increasing brain NAD+ levels—either by consuming a KD or by other ketone-enhancing treatments—might serve as a rapid and enduring strategy to halt or even reverse disease progression.

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Ethics Statement

This study was carried out in accordance with the recommendations of National Institutes of Health (NIH) Guides and Trinity College Animal Care and Use Committee. The protocol was approved by the Trinity College Animal Care and Use Committee.

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Author Contributions

ME, DNR, SAM and PS: conception and design of experiments; analysis and/or interpretation of data; drafting the manuscript; revising the manuscript critically for important intellectual content and approval of the version of the manuscript to be published. ME and DNR: acquisition of data.

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Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Acknowledgments

The authors would like to thank Ece Karhan, Susanne Bahnan, Kristina McMurry and Samantha DelVecchio for invaluable technical assistance.

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Footnotes

 

Funding. This research was supported by National Institutes of Health (NIH; NS065957, NS066392, SAM; AT008742, DNR), Trinity College, the Dorothy Goodwin Scholars Program—University of Hartford Women’s Advancement Initiative (ME, PS) and the College of Arts and Sciences at the University of Hartford (PS).

 

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Articles from Frontiers in Molecular Neuroscience are provided here courtesy of Frontiers Media SA

 

 

Edited by David Savage, 21 January 2018 - 01:28 AM.

[David Savage]

Measuring Ketosis with Niacin?

 

So...here's an idea that I've kinda been working with but starts to make more sense as I progress.

 

First off, I have in past measured ketosis with the pee strips.  Never really looked at the level, more so for just confirmation that I was actually in ketosis.

 

Anyways...there's always some chatter about "How Deep" of ketosis that you are in by this measurement of Ketones in your urine.

 

To me, this doesn't actually make a lot of sense - Depending on your goals for Ketosis...so, hear me out here.

 

My goals around a Ketogenic diet are for weight loss.

Nothing more...

 

So understanding the basic thermogenetic effect (Calories in/Calories out), the idea of consuming Massive amounts of Fat, butter or exogenous ketones really don't make a lot of sense.  If I have more ketones in my pee, it just simply means that I've burned more fats producing these ketones.  But if I am consuming globs and scandalous amounts of Fat, it actually makes sense to produce more ketones thus seeing larger quantities in urine.

 

Fasting - IF and Longer terms Fasts put you into a Ketogenic state.  Meaning that without consuming the 70-80% fats as a part of the diet, you still get into ketosis.

 

Aconita has touched on this in a few posts, not sure how deep he actually gets into this, but does show some ideas around a True Keto Diet and a Low Carb diet.

 

Effectively, this seems to be the case.

 

If the body is low on carbohydrates, it is forced to break down fat and produce ketones.  If your goal, like mine, is to lose weight...why not rely on your current fat stores, keep to a lower consumption of calories than your BMR and force your body into the Ketogenic state?

 

Maybe this has been covered...the internets is a big place full of information and miss information, only one thing being consistent is that where ever there is a New Idea for anything, there's always somebody waiting to capitalize on it by cannibalizing the idea and adding their own marketable product.  Since I am not selling anything and really not looking to buy anything, it seems that this may be a good place to either add onto this logic or dispell it.

 

Feel free to drop down your dos centavos.

 

ANYWAYS...

 

As mentioned before, the idea of taking Niacin at night is so that I get that FLOOD of ketones at night and am not trying to go through my day with the gas tank on empty.  Taking Niacin throughout the day, as I am IF and Low Carb isn't a pleasant feeling. 

 

Over the weekends and when I consume higher than usual carbs (by my own ideas), I take Berberine and will drop in additional Niacin.  

 

To me, this makes sense to get the carbs clearing the Liver as fast as possible and put them into the muscles/body where they can again be drained as fast as possible.

 

So...Friday - I had a few beers...or quite a few...whatever - Don't Judge me!

Friday Night - Took the double dose of Niacin and Berberine after dinner and unfortunately again - AFTER DERMAROLLING - OUCH!

Saturday am, I took the berberine and added in the Niacin to again work at mobilizing the carbs/glucose to not upset the state of ketosis.

 

Now, after the inital shock of still being in that Niacin unadapted state from the beers and getting a minor body flush, I started to feel that Brain Fog energy ZAP that I am used to getting if I take Niacin in a Fasted State.  

 

By Again, cutting off ketones and waiting for the surge to hit - as previously mentioned;

 

 

So ketosis is at first inhibited by niacin, and then comes in full force after a few hours.

 

Doesn't this actually provide confirmation of ketosis?

 

If we can appreciate that we need ketones for function, pissing them out is confirmation that we have more than we need.  If you look to confirm ketones by pee strips and it shows that you aren't in a state of ketosis, perhaps it just means that your body is using up all free ketones...right?

 

But if you confirm ketosis with Niacin and get the energy zap and brain fog, isn't this confirmation enough?

 

Ponderous...really, ponderous.

 

 

Edited by David Savage, 21 January 2018 - 07:30 PM.

[David Savage]

Now here's something completely unexpected from the weekend...

 

Let's start off with the previous Weekend and then move on to this.

 

The Friday before Last, I weighed in at 175, which was GREAT.  Don't even remember the last time I was at that weight and of course, celebrated that into the weekend, beers n wings n some other shitty stuffs...nothing as bad as a pizza, bread or cake, but shitty in relation to where I have been.

 

Come Monday, I had gained 3.8 pounds.  Given the beer consumption and leaking a little on the food thang, I had attributed this to water weight and by Tuesday had erased this gain.

 

Well...

Friday - Heavy weight training day - Legs suffered the most, even had issues with squatting on the toilet on Saturday/Sunday(TMI), and followed that up with a Cardio Cool Down - 1 hour on the Treadmill.  Friday weigh-in came in at 174.2 Pounds.

 

Over the weekend, around 24 beers, not much terrible in the diet with exception to some sauces added to my meals that had sugars added.  Did some Dragon Chicken on Friday, Wings on Saturday, both with some sugar-based sauces.  That being said, I still stuck to my 1 meal/day and kept steady on the Niacin.  Fully expecting to have again regained a little water weight, especially after being rather idle over the weekend, I just tipped the scales at 173!

 

WHAT??

 

How the fuck did I manage to put away 24 beer and not only NOT GAIN Weight, but actually lost 1.2 Pounds from my Friday weigh in?

 

The only thing that has really changed is my dosing of Niacin and not so much on the quantity but when I was taking it.

 

Is it possible that the Rebound effect of Niacin with FFA and Ketones during a rested state helped me drop that weight?

Am I still carrying the water weight from the beer and this is actual fat lost?

 

This will make for an interesting week on the scale.

 

No workout today, babysitting the granddaughter but will be back at it tomorrow.

 

Weekend Meals:

Friday:

Dragon Chicken Lettuce Wraps:

 chicken lettuce.JPG   121.23KB   0 downloads

 

Sunday:

Cheddar Bacon Chicken Breast - Boneless Skinless

Zucchini chips (that's what they are called, but I don't consider anything without a crunch to be a chip)

Coleslaw.

 Chicken and slaw1.JPG   119.21KB   0 downloads

[David Savage]

After dinner tonight, on schedule, I took my evening supplements as stated in the first post:

 

Evening:

Hyaluronic Acid - 750mg.

Berberine + Milk Thistle -375MG/ea - total 750mg cap.

Lysine - 1000mg.

Vitamin C - 1000mg.

Niacin - 1500mg.

 

Sans beer tonight, but I still received a bit of the dreaded Niacin Flush.

 

Hrmmmmm....

 

Over the weekend and with the beer, I had expected to see and feel some of this, but after clearing out figured I would be back to being Flush Adapted - or Flushless - or Niacin Adapated...whatever...

 

But it seems I'm not...

 

So, to get in this state of adaptation I took 4 fairly consecutive doses over 24 hours.  Now, I've dropped back to 2 doses - total 1500mgs and am no longer adapted.

 

Could it be that 4=/=2?

 

That would seemingly be the case.

 

After the flush effect was over, roundabouts 30 minutes, I decided to up my dose and go back to a 3000mg/24hr period dose.

 

What remains to be seen is if the flush will happen with my evening FULL dose tomorrow, or if I will need more/less on a Water Fast.

 

Re-read over some interesting information HERE, that would almost make me want to add in something to inhibit mTOR and keep my AMPK additive through the fast as well - Berberine...I do know the dangers of going down this road, take too much into consideration and my belly will be filled with capsules instead of taking advantage of a full Water Fast with only the Niacin.

 

 

 

Metformin, a drug widely used in type 2 diabetes, also activates autophagy but not through mTOR. It increases AMPK, a molecule that signals the energy status of the cell. If AMPK is high, the cell knows that it has insufficient energy and increases autophagy. AMPK senses the ADP/ATP ratio, thus knowing the cellular energy levels – sort of like a fuel gauge but in reverse. High AMPK, low cellular energy status. High AMPK levels directly and indirectly activate autophagy, but also mitochondrial production.

 

 

Mitophagy is the selective targeting of defective or dysfunctional mitochondrion. These are the parts of the cell that produce energy – the power houses. If these are not working properly, then the process of mitophagy targets them for destruction. The critical regulators of this process includes the notorious tumor suppressor gene PTEN. This may initially seem bad, remember that, at the same time that mitophagy is increased, new mitochondrion are being stimulated to grow. AMPK for example, will stimulate mitophagy as well as new mitochondrion growth – essentially replacing old mitochondrion with new ones in a renewal process. This is fantastic – essentially a complete renovation of the mitochondrial pool. Break down the old, junky mitochondrion and stimulate the body to build new ones. This is one of the reasons metformin is commonly promoted as an anti-aging compound – not so much for its blood sugar effects, but instead because of its effect on AMPK and autophagy.

 

 

Making me also wonder, would Berberine and something to inhibit mTOR be redundant inside a water fast?

 

[David Savage]

Welp, I think I found my answer to the whole Berberine and mTOR inhibitor...

 

Reading up on mTOR, depending on where you go and what you look at, it's a fucking terrible thing and thus the reason that people take mTOR inhibitors like Rapamycin...but in actuality, moderation may apply to this and the proper cycling might be beneficial.

 

Benefits:

mTOR allows us to put on muscles.

Increases ATP Production

Creates New Mitochondria

Increases Mitochondria Metabolism by activating PGC1a

 

Fuck, who'd want to suppress or inhibit these effects??

 

Answer - People that eat too much too often...

 

People that eat too much too often, are also looking for Skinny Pills...I know this, because I too have gone this route.

 

So, just spitballing here and as applicable to my PRE-WATER & NIACIN FAST and applied to my current IF program...

Berberine activates AMPK.  When AMPK is in the house, mTOR is inhibited.

If I am taking Berberine with my last meal of the day, I may be inhibiting the only time I can take full advantage of mTOR.

Seems defeatest, really...

 

SO...

 

Instead of taking Berberine in the evening and after my last meal, I am going to be cycling it through the day, getting the benefits from mTOR from my one meal per day and allowing autophagy (cleaning out the leftovers from mTOR) induced by this single meal per day fasting schedule and Berberine in the AM/Early afternoon to help with the Handsoming Effects.

 

I mean really, our bodies are pretty fucking smart.  They have all sorts of mechanisms that we have only begun to understand.  WHY would our body's have something like mTOR if it was more harmful than good?

 

Now, if you aren't on any fasting protocol, consistently overeat on the proteins, don't get any physical activity, maybe this whole mTOR thing is something you need to limit.

 

Seems to make perfect sense...now apply it and see where we go...

 

mTOR to help build muscles, increase ATP and mitochondria production while fasting in a ketogenic state to reduce fat seems like a PERFECT RECIPE for being more Handsome!!

 

As for the water fasting with Niacin, it seems to me to just keep to the original idea and leave everything else out of the equation.

 

 

[Believer]

The best way to lose weight is not to fast but to constantly consume carbs or starches.

Studies prove that starches cause the most weight loss, probably because they require more energy to metabolize for energy.

I have tested this again and again, fasting slows metabolism which has a large effect on reducing weight loss.

To keep metabolism going, produce thyroid hormones and etc., you need carbohydrates. Simple, quick carbs work the best whereas slow carbs tend to produce weight gain (as opposed to slowing weight loss).

 

I lost a lot of weight (800g to 1kg a day) consuming almost pure sugar (zero fat and protein) candy treats every 30 minutes or so. Although too much pure sugar seems to slightly slow weight loss down, so there is a balance between too much and too little.

 

As for fat on the belly, that's a MALE thing, that's what male hormones do to us although there is some evidence that stress hormones can also cause it.

We look for a flat belly in women because it signals to us that they have high activity of estrogen, which flattens the stomach.

 

 

[David Savage]

Mmmmmmmmmmm....Cold Beer!

 

Another week under my belt and off my beltline and time for some weekend refreshments!

 

Aaaaaaaaaaaauuuuuuooooooooooooga!

 

Lowest weight this week - 171, down another 2 belt sizes and only one hole left before this belt needs to be punched or punted.

 

I've had to make a couple of adjustments this week, due to not wanting to scrub the toilet EVERY FUCKING DAY!!

 

Wasn't sure if it was the Berberine or the Lysine, but something was making the belly a little crabby and thusly resulted in diarrhea that would pass through a coffee filter unchanged...Ack!

 

Took a day without the Lysine, tummy issues persisted.

Took the following day without Berberine and issues seemingly resolved.

 

Thankful for that...but now I seem to be a little Ketobunged up - Slow, but manageable.

 

Daily sups:

AM - Omega 3, Hyaluronic acid, Milk Thistle, Mucuna Puriens, Vitamin D, and Lysine.

Afternoon - Hyaluronic Acid Mucuna Puriens, and Lysine.

Evening - Niacin, Lysine, Magnesium, Melatonin.

 

This seems to be the keeper!

 

Hitting 3000mg of Niacin in the evenings seems to have leveled out.  Though I get the 'Crack Bug' itch, there's ZERO when comes to the flushing...happy about that.  In addition, given a daily work out regime, I've been able to keep to a fairly heavy protocol without breaking the 1 Meal/Day.

 

That being said, by the time the wife gets home and I get dinner on the table, I am fucking RAVENOUS!

&

That being said, my stomach capacity has dramatically decreased!

 

Last nights offerings - BBQ'd Flank & Twice Baked Cauliflower casserole - I was simply amazed at how full I got on a lot less than would have filled me a mere month ago.

 

As a huge Mash Potato guy, I typically eat a regular plate and then follow up with an entire plate of Tatoes.  Last night, had a few heaping tablespoons with a little steak, and though I made it through the plate, a second helping was barely choked back.

 

It was like this for the couple nights previously.

 

Taco Salad Night.

BBQ'd chicken and Coleslaw.

 

I ate a lot less than normally accustomed and still felt overfull when going to bed.

 

THIS IS AWESOME!

 

I've never really had portion control.  Never had that switch inside me that told me when I was actually full and typically just ate until all of the food was gone.  This definitely lead to some of my issues and most certainly how meals in our house grew from average family sized to "Who the fuck is all of this food for" sized portions.

 

Pizza Night - I would eat a Large to myself and dabble in the others.

Perogie Night - Would start off with 24 and see where I would go from there.

 

One meal/day - for the portions I cook vs what I consume leaves a fridge full of leftovers.

 

Meh.

 

Anyways...happy to actually be able to recognize when my belly is full and know that I can operate on significantly less than I used to.  

 

As for the Handsoming Effects...

 

Wrinkles have been fading - Helped by the Hyaluronic acid (I would assume) and a few daily applications of coconut oil on my face.  There's a lot of road left to cover, but starting to look more youthful.

 

As for the rest...

 

I have a NECK!!

I have a CHIN!!

 

Though...

 

Tried on some of my regular work clothes and even my daily wear jeans...Nothing fucking fits me anymore!!

 

Not long before the proposed water fast and I am already starting to have doubts.  Wanting to do this to get better on body mass, I seriously don't have that much left to go.

 

Skrawny=/=Handsome!

 

Will see how the beginning of next week goes.  Caloriewise, I am down to fractions of my previous and more honed in on being fat adapted...meaning a Fast should be a lot easier than my first go round.

 

Might have to take the Vanity out of the equation and just shoot for longevity?

 

 

 

 

[Believer]

You should never consume vitamin D without vitamin K2. If the vitamin D is in a high enough dosage to even have any effect (over 5000IU) then it will calcify your arteries.

 

As for weight loss, look up the studies, ignoramus.

Keto is a fad diet. It has positive effects but it simply will never be the quickest way to lose weight.

High starch > High quick carbs > High fat diet (keto) for WEIGHT LOSS.

 

No amount of downvoting or regurgitation will change reality.

[David Savage]

You should never consume vitamin D without vitamin K2. If the vitamin D is in a high enough dosage to even have any effect (over 5000IU) then it will calcify your arteries.

 

As for weight loss, look up the studies, ignoramus.

Keto is a fad diet. It has positive effects but it simply will never be the quickest way to lose weight.

High starch > High quick carbs > High fat diet (keto) for WEIGHT LOSS.

 

No amount of downvoting or regurgitation will change reality.

 

Oh you poor silly cunt...

 

You are most certainly victim of the Internet in your shortened attention span while being cursed with an obsessive-compulsive tendency.

 

Tell me, smart guy, when the last time you went out with your scale measurement posted on your t-shirt?

 

Like, instead of a "My Name is" tag, you wore a "My weight is" tag...

 

You don't.

Never happens.

 

Reason being, nobody gives a shit!

 

If you are looking to be lighter, certainly getting on a low fat, higher carb diet, even up to including a FULL starch diet like the potato diet will help you decrease the numbers on the scale.  This has undoubtedly been proven, time and time again...

 

But if you actually took any time to review the name of the header on here or any of the content, you'd see that my scale is only one of the metrics of what I am using to measure my progress.

 

It's vanity, fucker!!!

 

I want to look more handsome!

 

In doing this, my goal is not to appease the Scale Lords by dropping body mass by decreasing my muscle tone.  It's to have a more appealing outward impression.

 

The goal is to look more handsome!

 

If I burn off fat stores, I reduce my waist, shrink my pant size and the size of my ass, while still showing off a predominant muscular stature.

 

Is this making sense to you or would you like me to google that for you, you dizzy fuckstain?

 

Your time is better spent in the echo chamber of the ignorance of your culture.

 

Go find another thread to troll.

 

 

[Believer]

Okay, (((David Savage))) I understand.

For your info the keto Youtubers with big muscles who look "shredded" are on a ton of steroids.

[David Savage]

Okay, (((David Savage))) I understand.

For your info the keto Youtubers with big muscles who look "shredded" are on a ton of steroids.

 

 

I'm sure you have sources for this, right???

 

Whether you do or do not, it's still of no matter.

 

Reason being, I can retain muscle and burn fat by a state of ketogenesis.

 

Ergo...my path is dictated by my goals - my goals are significant of my path.

[David Savage]

Reason 538 to not be a Predominantly Carb Eating Fuckstain...

 

Don't get me wrong, the potato was AWESOME, and yeah, I know the starches are outside of the Keto Window...it's the weekend, I do get to afford a little latitude.

 

 Steak n T.JPG   249.42KB   1 downloads

 

2 Inch thick Ribeye!

Sous Vide - 140 F

Seared on the BBQ to Perfection

Garlic Butter Finish

 

Steamed Broccoli

 

Baked potato, sour cream and onions.

 

Oh Yeah, baby...That's what I'm talking about!

 

Try get that flavor out of a fucking Snickers Bar or Oreo.

[David Savage]

Meal of the day...

 

LC Lasagna!!!

 

Ground Chicken, homemade marinara, zucchini layers, with scads of parm and mozza.

 

 Keto Lasagna.JPG   142.33KB   1 downloads

 

Mmmmmmmmmmmmmm

 

Will serve with a side of Caesar Salad.