Bought some root ginger today, so that I can add this to my arsenal of potential fat burning things! It can’t do any harm, and I can easily spare the 1.8g carbs. Even if there is a minuscule fat burn with ginger, all these minuscule things add up! I’m all for trying something different!
@Mtb To get things going I recommend the first day eating 15-25 grams of ginger root spread out during the course of the day, with about 5-10 grams an hour before going to bed. Succeeding days you can cut back to 10 grams per day before bed. Let us know what happens! Thanks.
It’s glass and stainless steel cold brew thing but instead of coffee I use some grated ginger (easier to grate if frozen.) I’ve got ginger water at my fingertips now. Makes a nice night cap and I find I enjoy it MORE without alcohol to cut it.
I had a couple juice glasses full during a non eating day the other day, stomach handled it fine.
Tomorrow will be first weigh in. When I weighed this morning, I had not lost from the day before. On the previous three days, I had lost 0.4kg per day. I’ll post daily weight loss/gain. I’m really interested to see if there is a difference using ginger. I hope some of the other forum members report back with results using some of the different methods that were talked about. I’m especially interested in the ginger capsules if they have the same result.
Interesting. That looks like a regular ol’ teapot, but with a fancy shape. How do you make your ginger juice? How much ginger? Do you cold brew it?
So, chewed and swallowed 10g of raw ginger last night about 1.5hrs before bed. This morning, weighed myself to find I’d gone from 96.3kg to 97.3kg. a gain of exactly one kg or 2.2lbs. to be fair, I’m not surprised. Yesterday was a lot of exercise.
7 mile fast walk
Heavy chest and arms at gym
30mins cardio on elliptical machine
30 mins cycle spin class HIIT
So yes, my poor ragged muscles will be retaining extra fluid today.
Next results tomorrow.
It is more like a beaker It has fancy flexible gaskets to keep all the air in/out. Yeah, it’s fancy but in the end I guess it is a jar with a mesh strainer. Lol.
I just took some ginger out of my freezer stash (I got a couple of kilos of young locally grown ginger a while ago) grated it up and then filled the container with water. I filled the stainless steel strainer part about 3/4 with ginger but by the time I ran water over it it squished down to, like, a third. Then I put it in the refrigerator overnight. The resulting ginger water is nicely gingery/pale yellow but doesn’t … hurt. A half cup of loosely packed ginger to a liter of water?
I usually make ginger tincture, which is grated ginger in a jar covered with vodka and left for several months. That also is good.
To add feebly to the original purpose of this thread, I have lost 4 pounds in the last week, which COINCIDES with drinking ginger water but also with my second 48 hour fast so that confounds it.
Thanks, I’ll have to give that a try!
Also good to know ginger freezes well. My last batch sprouted because I forgot about it.
It grates really well when frozen, almost to dust size sometimes. I was doing that and throwing it into a cup of boiling water for tea this last winter.
I just chop the roots up and scatter them over my finished plate of food, same as I do with garlic. And chili. Seems perfectly digestible to me.
Ooooo! I does!
|Date||Weight||Fat||Lean||Fat% (Ref)||Fat% (Omron)||Fat% (Navy)||Fat% (Levl)|
As noted above, I upped my daily calories from 2700 to 2800 on June26. I had been eating about 10-15 grams of ginger root each evening for the past several days and feeling hungry each morning. I do not want to lose weight, so I upped my calories to prevent it.
As you can see from the above weigh-in data, in the 9 days since June 27 I gained net 3 pounds, but lost 3 pounds of fat mass. Or so the Navy online calculator tells me. I expected to gain some weight, but the fat loss was unexpected.
Relevant. This past week I have been sick with a chest cold. To try to beat it, on Wednesday I ate about 35-40 grams of ginger root during the course of the day. Doing so did not bump me out of ketosis, but it did push my carbs up to about 30 net grams for the day. I have eaten none since then (Jul03-06).
- 'Ref' fat% is fat weight divided by total weight
- 'Omron' fat% is derived from my Omron HBF306 impedence device
- 'Navy' fat% is the result of the Navy online calculator
- 'Levl' fat% is the result of the Levl online calculator
- Jul13: still sick, starting Jul07 ate ginger root daily (15 grams), still hitting my daily calorie target of 2800, morning hunger has disappeared; I missed two work days this past week (Wed & Thu), so level of activity has dropped
- Jul19: still sick, but getting better finally; cough won't let go. Still eating ginger root daily (15 grams), still hitting my daily calorie target of 2800, although I undershot by 200 calories one day. Does not seem to have mattered. 5 days of work in a row, so level of activity has increased nearly to normal. Had off today, starting tomorrow 4 days in a row.
- Jul26: last ginger root last night for a while. If my premise is correct, and I hit my 2800 calories daily for the next week, I should start to gain some weight.
- Aug02: I hit my 2800 calories (or close enough) daily for the past week, except for a couple days. I'm back to the same numbers I had Jul 19 except for the Omron fat% which is slightly different, but still up. Significantly, fat% went up a bit except for the Levl calculation, which I think is the least accurate of the three.
- Aug09: The Omron fat% is much lower than both the Navy and Levl numbers. Maybe there's less fat in my arms. I've hit my 2800 daily target, or close to it, every day of the past week. I've gained a pound, apparently mostly lean mass.
- Aug16: The Omron fat% continues lower than both the Navy and Levl numbers. I've discovered that the Levl calculator allows fractional numbers, which is good to know. The Navy calculator rounds up/down to the nearest whole number. I've hit my 2800 daily target, or close to it, every day of the past week except for a couple. I've lost a pound, apparently mostly fat mass. The only thing I've done differently from previous weeks has been to repair my bicycle and ride a couple of times.
- Aug23: The Omron measures impedence in my arms and upper body, mostly through the shoulders I presume. The Navy and Levl online calculators include both waist and neck measurements. The big change this week from last was that my waist measurement increased from 31+ inches to 33 inches. I managed to hit my calorie target every day and a couple days a bit more. So it looks like I added some visceral fat even though my total weight did not change.
What if "Eating to Satiety" ain't enough to reach prudent caloric targets?
Can we please stop repeating the “You have to eat at a deficit to lose weight on KETO” lie?
Can we please stop repeating the “You have to eat at a deficit to lose weight on KETO” lie?
I followed through to the Nikoley article and his references. (some of his references were about MCTs and fasting or severe calorie restriction)
Let me summarize:
BrAce is measuring ketones produced from fat coming out of fat cells unless you are using MCT-rich fats (or in some cases SCFA which produce a small amount of ketones in the gut). Whether there is a net gain or loss from those cells is a different matter and is where energy balance comes into play.
I’ll add on by describing what the limiting steps are - because the more I write this stuff down, the more I can keep it sorted in my head.
Long chain dietary fat must first be cycled through adipose before going to the liver as FFA. FFA leaving fat cells depends primarily on the health of the fat cell - its ability to respond to insulin - and insulin levels acting on the GLUT4 transporter. Lower insulin = more fat released. Once FFA gets to the liver via the bloodstream, some of it is used and the remainder is re-esterified and exported as cholesterol in VLDL. Of the fraction that makes it to be metabolized, it must first be able to cross into the liver mitochondria. That step is rate limited by carnitine (CPT1), which in turn is regulated by other factors in accordance with fed/fasted status.
Now we’ve made it into the liver mitochondria where beta oxidation happens. (yay!) Whether or not ketones are produced is determined by whether or not oxaloacetate (OAA) is depleted thus halting the Krebs Cycle which produces glucose as an end product. This is accomplished by overwhelming the available amount of OAA with the acetyl-CoA produced by the cleaving of the influx of FFA into smaller chunks, producing Acac. After that, the relative amount of Bhb or Acac produced is determined by the NAD+/NADH ratio.
So, other than ginger potentially increasing the amount of FFA released from fat cells, thus overwhelming OAA, I wonder which other mechanisms in may involve?
I’ve looked through some ginger studies and there’s a couple things that I don’t get as far as how it is beneficial for fat release.
- Ginger is said to reduce glucose by increasing insulin (genetically modified rats).
- Ginger can act on GLUT4 transporters independent of insulin to clear glucose. I don’t see how this helps get fat out of the cell.
- It’s anti-inflammatory properties may help in the cytokine signalling produced by adipose tissue. This also works with NAFLD.
I’m going to attempt to answer my own question.
Adiponectin, an adipocytokine, increases hepatic fatty acid oxidation by inducing PPAR-a and AMPK
So… by correcting the adiponectin signal from inflamed adipose tissue, it encourages fatty acid acid oxidation in the liver. (NEFA = FFA) I think they mean it lessens the creation and export of VLDL (normal) and/or storage of TG in the liver (pathological).
This mechanism would increase ketones by metabolizing a higher percentage of FFA available in the blood and lower cholesterol.
I found something else that works against PPARa:
PPARα is activated by natural eicosanoids derived from arachidonic acid via the
lipoxygenase pathway, such as 8-S-hydroxytetraenoic acid (8-S-HETE)21 and leukotriene
B4 (LTB4),23 https://nyaspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.2002.tb04258.x
Which is interesting because, ginger acts similar to NSAIDs and they both interfere with arachidonic acid. Ginger blocks both COX and 5-LOX pathways.
ginger also suppresses leukotriene biosynthesis by inhibiting 5-lipoxygenase. This pharmacological property distinguishes ginger from nonsteroidal anti-inflammatory drugs. https://www.ncbi.nlm.nih.gov/pubmed/16117603
So, what are we to make of this conflicting action on PPAR (in the liver and elsewhere), which is the methodfor increasing FFA oxidation?
Also, PPARs are involved in other important things like fat cell differentiation (and that’s just the tip of the rabbit hole)
@carolT Thank you for your investigation, please continue! Meanwhile I will continue my experiment. As it looks like I am finally over my illness of the past 3 weeks, I expect my BrAce measurements to go back up to where they were prior. Today, for instance, I already got a 60ppm reading! The previous high for July so far was back on Jul 01 at 40ppm before my illness really kicked in. Since (while ill), BrAce readings have been mostly in the 10-20ppm range, with some fluctuations into low 30ppm and below 10ppm, but did not go to 5ppm or below.
If I remain free of the illness for the next week, I will eliminate daily ginger root to see what happens. If in fact ginger root is somehow increasing fat burn, then I expect to gain weight when I stop taking it.
Interesting about BrAce connection to FFA release from adipose rather than direct synthesis of ketones. My understanding is that Acetone is a break down product of acetoacetate rather than related to FFAs. So I look forward to further understanding that relationship. Interestingly, times when I would expect BrAce to be high, with increased activity burning more fat/ketones, it’s lower: during the day. While when I would expect it to be low, after reduced activity late in the evening and early morning, it’s high. It’s almost like there’s an inverse relationship, which would make sense if my energy is coming primarily from FFA burn rather than ketone burn. Unless I totally don’t understand what’s going on.
Yes, but acetoacetate production is directly related to FFA release and metabolism. I abbreviated it as Acac in my above description. (sorry) Anyway, it is the end product of a long line of things that have to go right in order to produce ketones at all. In general, the anti-inflamatory effects (and adiponectin mediation) are what’s increasing fat metabolism in the liver, leading to AcAC and spontaneous production of acetone.
I’ve been letting this simmer in the back of my mind for a bit and I found a nice diagram that isn’t overly complicated or overly simple IMO. I usually understand concepts better with a nice diagram to stare at.
The source of breath acetone is where the acetoacetate travels in the bloodstream to peripheral tissues. It spontaneously breaks down to acetone plus CO2, with a half life related to a bunch of things like temperature etc. The liver produces but does not use ketones. The muscles can use ketones but cannot produce them, so there is a constant flux between liver and other tissues during ketogenesis.
If acetoacetate gets used before it degrades, less acetone in the breath. Conversely, a bunch of it in the breath means you’re using less that you produce per given half life of the molecule. I see a large increase during fasting because supply exceeds demand.
Back to my investigation into PPAR and its function in this cycle… I believe ginger acting by reducing inflammation modulates the oxidation of fat in the liver. I also think the method it uses to do this results in a reduction of cholesterol (trigs, VLDL therefore LDL) which is one of the things I see mentioned in some studies.
My concern at this point is whether or not we are seeing a statin-like effect with long-term use. The mechanisms involved look similar to me but I haven’t gone deep enough to know for sure. Short term effects may trump longer term concerns, or the dose may make the difference. Correct function of PPAR alpha is critical in the beta oxidation pathway, and genetic problems in this area can be a reason keto won’t work for some people.
Thanks for that! You’ve explained my observations that BrAce seems to be in an inverse relationship with intensity of activity. The more active I am, ie burning more fat/ketones, the less unused acetoacetate is around to break down into acetone. The less active I am, ie late evening, overnight, early morning, the more acetoacetate breaks down simply because there’s more of it floating around doing nothing much.
So in fact, rather than tracking ketones specifically, RER may be a better way to determine how efficiently the system is working, assuming with @Karim_Wassef here, that Lumen or something similar turns out to be an accurate tool for home measurement:
As for ginger root mimicking statins, I wonder about that and hope your investigation finds an answer. Just off the top of my head, though, in Asia ginger root has been used for centuries, possibly millennia, for nutrition, health, weight loss and probably other reasons. If it had any actual negative consequences I think they would have discovered them by now. Of course, I could be wrong.
That just might explain BrAce ‘spikes’. My first, discussed here, occurred on a sunny, hot day - so physical heat. The second, this past Saturday morning (to over 60ppm), occurred after a rather animated discussion between myself and one of my Walmart managers over my shift time for the day - so emotional heat.