Mocha Walnut Brownies

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . .  . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.

8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)

Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.

Comments (11) -

  • Stephanie KL

    1/2/2012 5:54:10 PM |

    Does your pan need greasing prior to adding the batter?

  • Jennifer

    1/2/2012 8:16:40 PM |

    They look great, and I'll bet they are darned tasty, but you are also serving yourself a load of PUFAs with these and then you want to top them with more yet.  One brownie, maybe.  Two or three, no way I'd eat that much PUFA, even if it's coming from nuts and not corn or soy oils.    I don't mean to come across as a twit about this stuff, but if you are a "person in a certain metabolic state", like me,  then you have to really look close at these kinds of things.

  • Might-o'chondri-AL

    1/3/2012 11:45:22 PM |

    For Laura (continuation from previous Dec. 2011 thread "Are you hungry"),
    Assume very  low carb & paleo styled dieters are going with high dietary fat to complement reasonably high protein yet some feel weight loss is not enough. Dietary fat is more than a molecule glob we just act on and has signaling properties for our cells. We synthesize distinct fat molecules inside us from different dietary fats by splitting some apart & elongating into new forms.

    Palmitic acid ( palmitate) is what I suggest as involved in stalled weight loss for low carb & paleo dieters since admonishments to eat more fat don't isolate the types of fatty acids metabolic signal cascades. De-novo lipogenesis from carbs forms palmitic fatty acid but some may benefit from restricting other palmitate sources.  68% of the fat "burned" is usually palmitic acid.

    A mitochondria inside a cell has 2 mitochondrial membranes and to "burn"  most fat (like palmitate) inside that mitochondria  2  molecules are involved. A carnitine based enzyme (carnitine palmitoyl transferase, CPT) can only shunt  fatty acid like palmitate into place for "burning" when there is a free unbound CoA (co-enzyme A) to work with.

    A high fat diet frequently ties up +/- 90% of cellular mitochondrial CoA with fatty acid acyls (as acyl CoA). Coconut oil is only 7-10% palmitic acid and some of the coconut oil's other fatty acids do not need carnitine (CPT) to get into place for "burning" inside a mitochondria. In other words coconut oil fatty acids get "burned" promptly and it doesn't tie up much CoA, which leaves more " free" CoA for other fatty acids to use in order to get into place for "burning". This is part of how coconut oil boosts fatty acid oxidation.

    High protein intake (over time, not as a single meal response) influences the mitochondria;  but let me specify first how it affects skeletal muscle mitochondria. In the inner mitochondrial membrane there is uncoupling protein 3 (UCP3) that is upregulated from a high protein diet. The U.N.'s WHO sets minimum daily protein requirement at 0.85 gr protein/kg. body weight & thus 1.7  - 2.0 gr protein/kg. body weight is a practical description of  high protein  (note: chronic kidney disease and some medical conditions are decidedly not suitable for high protein intake).

    Skeletal muscle UCP3 doesn't work to lower a mitochondria's membrane potential and as such doesn't make that cell use more oxygen. UCP3 causes a type of "uncoupling" whereby it "spills" some protons from the mitochondria's electron transport chain of ATP energy production and results in fatty acid anions (ie: fatty acid hydrolyzed be mitochondria UCP3 splits off a proton). Then that fatty acid anion can fit being shuttled back out from inside that mitochondria to ease the mitochondrial fatty acid burden.

    The effect here, from high protein increasing UCP3 expression, is to "free" up a CoA for each fatty acid shunted out and this then gives that mitochondria more "free" CoA that can then be put to  work with a carnitine enzyme (CPT) to put some of the backed up fatty acid load into position for "burning" to make ATP energy. This is part of how high protein diets increase fatty acid oxidation in skeletal muscle.

    Now, back to palmitate as a dietary fat; consider these food choices where 150 gr. liquid non-fat Kefir = 18 mg. palmitic acid vs 150 gr. liquid regular milk = 1,500 mg & then also compare 150 gr. of cooked garbanzo ( basis of hummus) = 300 mg. palmitic acid vs 150 gr. beef jerky (an example for solid meat protein) = 1,800 mg. palmitic acid. Since when one is trying to lose weight often the desired fat tissue signalling lipo-kines are not doing what normally would .

    Dieters adipose tissue often begin with altered lipo-kine expression and demonstrate multiple gene expression peculiarities that persist even when they have already lost a good bit of weight. Palmitate is implicated, for example, when low circulating adiponectin levels are problematic.

    Aside from the negative effects of the palmitate derivative ceramide (not detailed here) there is the risk that high palmitate interacts with the local inflammatory cells' TLR4 (toll like receptor) engaging NFkB (nuclear factor) causing that cell's enzyme NADPH oxidase to generate excessive reactive oxygen super-oxide molecules. One unknown is whether an individual is vulnerable to any side effect(s) or if  local tissue responds "normally" to elevated levels of palmitate by using the super-oxide spun off as a signaling molecule for a proper metabolic response.

    One concern is that some people with elevated palmitate might get increased endoplasmic reticulum (ER) stress ( ER inside cell is where proteins must fold properly). Doc's readers know we vary in ApoE genetics; and some ApoE isoform % heritage is one reason high palmitate makes them more prone to induced ER stress in certain tissue cells.

    Hunter-gatherer & pastoral people respond to high fat diet with sleekness because high saturated fat over time (not a meal) causes the mitochondrial membrane (paradoxically) to actually become higher in % of polyunsaturated fatty acid (PUFA) content than a low saturated fat intake does. Anyway the result is a more flexible mitochondrial membrane for responding.

    Their proclivity toward high fat fuel "burning" (hunters prefer the fattest parts & herders get lots of milk fat) initially makes that mitochondria put out  lots of super-oxide which becomes a hydroxyl radical that snatches an atom of hydrogen from a PUFA  in that phospho-lipid mitochondrial membrane. Then that metabolite becomes a carbon cored fatty acyl free radical which the cellular oxygen makes into a per-oxyl, which becomes a substrate for spinning off molecules called alkenals (ex: 4-hydroxy-nonenal).

    In the liver (and some tissues) a different type of UCP in the mitochondrial membrane "normally" responds to the alkenal signal  & then UCP 2 "uncouples" to varying degrees of severity so that protons shunting through the electron transport chain (ETC) "spill" protons. In this case the result of upregulating UCP2 in the liver due to a high fat diet is to make the ETC lose efficiency (due to "spill" lessening proton force ) and  that mitochondria must use more oxygen working more to churn out the correct amount of ATP downstream. If one's genetics somehow stymie the increase in UCP2 in any one of the tissue groups with UCP2 function in that inner mitochondrial membrane then high fat intake itself doesn't necessarily trigger this beneficial adaptative response.

    The "normal" side effect from this in the liver cell is reduced mitochondrial  membrane potential from the UCP2, but increased "burning" of fat there; so the hunter (or pastoral) stays sleek because this set up tends to make one lose weight and also keep liver metabolic rate up as they age.  Meanwhile UCP2 alters the dynamic so that less ROS is generated at the mitochondrial staging complex 1; it is a type of self regulatory feedback arrangement where the signal is in reaction to high fat intake. I suspect epigenetic insults to UCP2 may also confound the efforts of some dieters.

    To complete the picture it is relevant  that a high protein diet also upregulates UCP2 acting in key mitochondria; although skeletal muscle UCP2 is not as strongly influenced by high protein diet and it has more response with UCP 3 (skeletal muscle has more of it to begin with) . Our ancestors were feast or famine prone and caloric restriction is another factor which increases both UCP 2 & UCP 3 levels. Thus agriculturists which didn't/don't over consume usually stay slim despite carb based diets & more carb driven de-novo lipo-genesis of palmitate ( with Doc's supplements my labs are good seemingly eating  120+ gr. carbs daily).

    If I were stalling on  low carb/paleo-ish diet I would consider adding in olive oil because the oleic acid counter-acts the action of  palmitate (ex: eat hummus made with olive oil).  Cutting back on palmitate intake conceivably could be off-set by experimenting with more coconut oil (not to be confused with palm oil)  and/or adding in more select nuts/seeds for fat. I would also break ranks with theory and try a protein spell without animal/fowl fat by substituting casein (ex. fat free kefir/yogurt quark) & fish (while keeping up fish oil) & moderate daily portion of hummus to keep protein high (assuming no health contra-indication).

    Excessive (moderation is an individual variable) intake of alpha linolenic acid (ALA) actually decreases the amount of circulating DHA long chain PUFA synthesized and makes less available to incorporate into the cellular membranes. The role of DHA in cell membranes is beneficial for metabolic signaling ; membranes are not just casings of a uniform bagging. So replacing dietary palimitic acid fat with almonds (no ALA, 9% saturated) or sesame tahini (no ALA, 13% saturated), as opposed to loading up on flax (57% ALA, 9% saturated) or walnut (7% ALA, 16% saturated ) or canola (10% ALA, 6% saturated)  for fat may help contribute to other fatty acid signal cascades that might bump one past a weight stall even if already taking maximum fish oil.

  • Dr. William Davis

    1/4/2012 1:40:30 AM |

    Depends on your pan, Stephanie.

    I usually do not and it comes out just fine. If you are uncertain, coconut oil works best.

  • lola

    1/5/2012 4:54:42 AM |

    WOW - I am going to have to read this multiple times to absorb.. ha - but thanks... interesting

  • Ronnie

    1/6/2012 12:31:26 AM |

    I know low carb is the way to go for all genotypes, including Apoe 3/4 people.  But I've read that LOW fat is also necessary to lower heart disease risk for these 3/4's, not moderate fat.  Do you agree?

  • the internet

    1/9/2012 5:01:47 PM |

    ronnie, you cant go low fat and low carb simultaneously

    a diet that was 80% protein would kill you

  • Judd

    1/16/2012 10:34:02 PM |


    Just made these brownies.  Seems like the recipe could use less flour in order for it to be not so firm and dry.  Or increase the amount of coconut milk in the recipe.  I had to use a whole can of coconut milk and some water and regular milk as well to make the consistency to where I could spoon it into a pan.  Tastes and smells great so far...Thx


  • Judd

    2/9/2012 3:08:24 PM |

    Can''t get these to come out right.  Too dry even with half the amount of flour.  As soon as I add the egg chocolate mixture to the dry, it just all drys up.  Any bakers or ideas out there??

    Thanks, Judd

  • Dr. William Davis

    2/12/2012 2:56:45 PM |

    Try adding more liquid, e.g., sour cream or coconut milk, until you get a moldable dough consistency.

  • Eric C

    2/14/2012 1:58:19 AM |

    Dr. Davis,
    I''d like to add to the PUFA (aka: nuts) restriction argument here. When I initially started low-carb, I ate a lot of nuts. But nuts have a few problems:

    1. Copper
    2. PUFA
    3. Phytosterols

    There are more problems. But increasing copper & PUFA levels in the body causes big problems in the long-term since these two react so readily. After a year or two of eating maybe 50-100g of various nuts per day, my congenital bicuspid aortic valve developed a murmur and mild heart enlargement due to my aortic valve becoming moderately-severely stenosed. The cardiologist I visited thought I would need surgery and/or "wouldn''t make it past 40" without surgery. But I changed my diet. After increasing my grass-fed butter (saturated fat), beef tallow, etc. (low omega-6) fats and restricting PUFA to a bare-minimum (in addition to a few other things, though), the murmur is actually going away. It''s almost gone. I''m only 30, though. I can''t believe it. I was in serious condition just by eating 50-100g of various nuts per day... (odd since most studies show "benefit" on HDL/LDL). But now I''m realizing that despite an improvement in ratio of HDL/LDL, nuts increase lp(a) and oxidized LDL in the long-run like no other.

    PUFA''s are dangerous in excess. I avoid them like the plague now.