I can't see any massive sell walls yet, but they will probably appear in a couple of weeks.

Nobody is trying to drop the price, it's just a normal market behavior. You got spoiled by Markus and Willy who
prevented the early 2013 bubble from deflating to 30$ or below and then used more fake million $ to build the new bubble
much faster and higher than normal. Now the disillusioned market has to find THE bottom, and hopefully without manipulation.

IMO it's likely to test support at 320$ soon, and a dead cat bounce to follow, then test 275$.
I have checked the current market movements against those of October - November 2011, when a crippled start of wave 1 resulted in a double bottom at ~2$.
And I found that the current market is bearisher than that, so my most probable scenario is that we are still in wave C.

5m MACD of Chinese exchanges suggests another drop is possible soon.

Permabulls were "right" again, there was coiling, but for the other direction. However, the epic part is yet to come, this is just the prelude.

Remember this? It has been invalidated. Now the bullish scenario is to test support at 275$ on huge volume and bounce for good.

Not yet, maybe at 200$. Just wait...

Changed your mind?

You can't save a fish from water, nor a hodler from missing huge profits. Anyway:
https://www.cryptocoinsnews.com/bears-win-bitcoin-price-battle/

I do expect to see some green dildos after hitting support at lower levels, maybe like 320$. But that won't last long, testing 275$ is a must now.

And it didn't take much red volume to break support, I wonder what will happen with large volume.

The fed transactions may have made an impression in BDD too. If not, then could be more early adopters cashing out.

Now that the bitcoins from the auction are being distributed, question is if some of the buyers decide to dump
on exchanges, would they on mainland China ones? I think not, probably they would dump on Western exchanges like Bitstamp.
Which Bistamp needs to do some catching up to the Chinese, in order to regain it's real name of Bearstamp.

Chessnut, I think it's time to let go of the "trending toward 2450" scenario and think about the next local bottom, 2100 or 1950?

This is just the beginning.

This flip is specific to Bitstamp, but China leads the market. Since OKcoin data is missing for the last 8 days
from bitcoincharts, I can only see BTCChina which probably follows OKcoin, and PSAR didn't flip there.
Even if it would flip, it wouldn't mean what the OP implied, that a mania phase of the bubble is near.
For that, considering that the market moves about 4x slower than in 2013 (when Markus and Willy faked it),
we need 4w PSAR to flip (which is not available on bitcoincharts), in order to confirm an upcoming parabolic rise.

Surprise surprise, it broke down. Was sooo hard to see...

If the market would be preparing to go up we would see sustained buying, not crappy volume. The triangle should resolve soon, IMO down.

Sideways may end soon:
https://www.cryptocoinsnews.com/bitcoin-bulls-bears-fighting/

Ahem... quoting from Wikipedia:

As a neurotoxin, ethanol has been shown to induce nervous system damage and affect the body in a variety of ways. Among the known effects of ethanol exposure are both transient and lasting consequences. Some of the lasting effects include long-term reduced neurogenesis in the hippocampus,[96][97] widespread brain atrophy,[98] and induced inflammation in the brain.[99] Of note, chronic ethanol ingestion has additionally been shown to induce reorganization of cellular membrane constituents, leading to a lipid bilayer marked by increased membrane concentrations of cholesterol and saturated fat.[46] This is important as neurotransmitter transport can be impaired through vesicular transport inhibition, resulting in diminished neural network function. One significant example of reduced inter-neuron communication is the ability for ethanol to inhibit NMDA receptors in the hippocampus, resulting in reduced long-term potentiation (LTP) and memory acquisition.[45] NMDA has been shown to play an important role in LTP and consequently memory formation.[100] With chronic ethanol intake, however, the susceptibility of these NMDA receptors to induce LTP increases in the mesolimbic dopamine neurons in an inositol 1,4,5-triphosphate (IP3) dependent manner.[101] This reorganization may lead to neuronal cytotoxicity both through hyperactivation of postsynaptic neurons and through induced addiction to continuous ethanol consumption. It has, additionally, been shown that ethanol directly reduces intracellular calcium ion accumulation through inhibited NMDA receptor activity, and thus reduces the capacity for the occurrence of LTP.[102]

In addition to the neurotoxic effects of ethanol in mature organisms, chronic ingestion is capable of inducing severe developmental defects. Evidence was first shown in 1973 of a connection between chronic ethanol intake by mothers and defects in their offspring.[103] This work was responsible for creating the classification of fetal alcohol syndrome; a disease characterized by common morphogenesis aberrations such as defects in craniofacial formation, limb development, and cardiovascular formation. The magnitude of ethanol neurotoxicity in fetuses leading to fetal alcohol syndrome has been shown to be dependent on antioxidant levels in the brain such as vitamin E.[104] As the fetal brain is relatively fragile and susceptible to induced stresses, severe deleterious effects of alcohol exposure can be seen in important areas such as the hippocampus and cerebellum. The severity of these effects is directly dependent upon the amount and frequency of ethanol consumption by the mother, and the stage in development of the fetus.[105] It is known that ethanol exposure results in reduced antioxidant levels, mitochondrial dysfunction (Chu 2007), and subsequent neuronal death, seemingly as a result of increased generation of reactive oxidative species (ROS).[29] This is a plausible mechanism, as there is a reduced presence in the fetal brain of antioxidant enzymes such as catalase and peroxidase.[106] In support of this mechanism, administration of high levels of dietary vitamin E results in reduced or eliminated ethanol-induced neurotoxic effects in fetuses.[8]

  Did you mean "the next 5 hours"?